The macular is the central part of the retina and is the area where the fine detail of sight is formed so it is very important. Sometimes the macular degenerates blurred vision occurs. This is often the first sign that something is wrong with the eye. Distorted vision is also a symptom and if either of these conditions occur you should visit your nearest doctor as soon as possible. The condition can be treated, but like all illnesses, the quicker it can be caught the better. If left completely untreated macular degeneration can lead to blindness.
It isn't completely accurate to refer to just one condition known as macular degeneration. In fact there is dry age related macular degeneration, and wet age related macular degeneration. Dry AMD develops very slowly and is caused by the light sensitive cells breaking down as described above. Wet AMD is much rarer and is more serious too as it is more likely to lead to complete blindness if not treated.
This occurs when the blood vessels in the eye begin to grow at an abnormal rate. This growth forces the retina away from the eye wall and this detachment is extremely serious and will eventually lead to blindness. The signs of wet AMD are seeing straight lines as slightly curved and medical attention is vital immediately.
There are treatments available for both these conditions. Dry AMD is the much less serious condition of the two, and even making a few lifestyle changes can go some way to keeping the condition from worsening. Dry AMD occurs through the aging of the eye, so you can slow this down considerably by making your eyes more healthy and strong. This can be done through making healthy lifestyle changes and carrying out special eye exercises too. The condition can be slowed right down with simple changes to your everyday life such as these. Eating plenty of vegetables that are rich in vitamins and minerals is vital too.
If the condition is in the early stages then the eye doctor may well prescribe a course of injections with an anti-vascular endothelial growth drug. If the condition is too advanced or if these drugs do not help the problem then laser treatment may be able to stop the progression of the problem, although it cannot return vision that has been lost.
Eye surgery is quick and painless and the recovery period is short. That makes it a viable option for many people. Whilst the cost of such a treatment was extremely high many years ago, today the price is much more affordable. Because it is able to halt the growth of problems, it is extremely popular and has helped thousands of people across the UK. Regular check ups are absolutely vital if you want to catch any problems such as this early on.
There is a selection of macular degeneration treatment available and your eye doctor will prescribe that which is the most appropriate. Laser vision correction surgery is an effective way to restore sight and prevent the condition from worsening. Laser eye surgery can be used to treat other conditions too for example it is highly effective in cataracts surgery.
Showing posts with label macular degeneration association. Show all posts
Showing posts with label macular degeneration association. Show all posts
Friday, January 28, 2011
Sunday, January 23, 2011
Stargardt Macular Degeneration
By: Macular Degeneration In General
One of the more popular juvenile macular degeneration is the Stargardt Macular Degeneration. This category of macular degenerationi was first reported in 1901 by a German ophthalmologist, Karl Stargardt. It has the common feature of loss of central vision. In 1963, France ophthalmologist Adolphe Fransceschetti used the term Fundus flavimaculatus for a degenerative loss of central vision, but soon to be identified as Stargardt Macular Degeneration by Hadden and Gass in 1976.
This macular dystrophy affects about one in every 10,000 children. The problem may start anytime between the ages 6 and 20, but patients may not notice until they reach their 30s or 40s. First, the children may experience difficulty in reading, and complaining of some blind spots that are often gray, black or hazy at their central vision. They will need more time to adjust between the different lighting of the room too, between light and dark environments.
The dystrophy affects the retina, that sensitive tissue that lies at the back of the eye, focusing especially in the middle region called the macula. The macula is where focus is, that area that is highly sensitive and strong enough to give us the sharp central vision for tasks such as reading, driving and recognising faces.
Stargardt macular degeneration is similar to dry macular degeneration, with the build-up of abnormal yellow pigment substance called lipofuscin building up in cells underlying the macula. Patients will also experience problem with night vision, and it will be difficult for them to move around in places with low lighting. In some others, the patient may also experience colour impairment at advanced stages of the disease.
Vision loss is usually slow, until the 20/40 level. It may suddenly shoot right up to 20/200 where the patient is considered legally blind and forbidden from driving. In some cases, it may even deteriorate to 10/200 within a matter of months.
Genes are a big issue when it comes to Stargardt macular degeneration. A group of genes collectively known as the ABC genes, was found to be the culprit of this juvenile macular degeneration, a discovery made since 1997. The ABCA4 gene, responsible for the production of protein used as an energy transport to and from photoreceptor cells in the retina, mutates and produces dysfunctional protein that cannot perform such transport function. The useless ABCA4 protein then allows the accumulation of yellow, fatty material to accumulate in the retina, slowly covering the macularand ultimately causes the loss of vision. However, more studies had to be done to further understand how the mutated genes affect the biochemistry of the retina.
All is not lost for patients with Stargardt disease. It was found that patients may slow down the progression of vision loss by wearing UV protective sunglasses and avoid exposure to bright light. Although there is not yet any effective treatment for this form of macular degeneration at this moment, it is believed that the identification of the genes behind macular degeneration will help the search for new strategies and therapies. The latest is a study scheduled to begin in 2011, for the injection of embryonic stem cells into the eyes of twelve patients affected by the disease. The Advanced Cell Technology announced in November 2010 that the FDA had approved this injection and study.
Stargardt Macular Degeneration may be either autosomal or recessive trait type. A person may not have prior family history, but may have a recessive gene. If both parents carry a mutated gene, there is always a chance for the child to develop macular dystrophy. In fact, there may be more than one family member who gets Stargardt. For children who did not develop Stargardt, there is again the possibility of carrying the mutant gene, and pass on to their children instead. The chances will be 25%.
Three tests are used to check the presence of fundus flecks and the loss of cones to determine whether a patient has Stargardt Macular Degeneration. It may be fluorescein angiography, electroretinography or electrooculography. Since this problem is rare, it is not a widely studied subject. The discovery of genetic mutation in Stargardt may have encouraged the findings of genetic links for age-related macular degeneration, but further studies on the age-related macular degeneration may also become the contributing factor towards better understanding of Stargardt’s disease and its possible lead to new treatment. Whichever way it may be, it will always remain hopeful for parents and their affected children.
One of the more popular juvenile macular degeneration is the Stargardt Macular Degeneration. This category of macular degenerationi was first reported in 1901 by a German ophthalmologist, Karl Stargardt. It has the common feature of loss of central vision. In 1963, France ophthalmologist Adolphe Fransceschetti used the term Fundus flavimaculatus for a degenerative loss of central vision, but soon to be identified as Stargardt Macular Degeneration by Hadden and Gass in 1976.
This macular dystrophy affects about one in every 10,000 children. The problem may start anytime between the ages 6 and 20, but patients may not notice until they reach their 30s or 40s. First, the children may experience difficulty in reading, and complaining of some blind spots that are often gray, black or hazy at their central vision. They will need more time to adjust between the different lighting of the room too, between light and dark environments.
The dystrophy affects the retina, that sensitive tissue that lies at the back of the eye, focusing especially in the middle region called the macula. The macula is where focus is, that area that is highly sensitive and strong enough to give us the sharp central vision for tasks such as reading, driving and recognising faces.
Stargardt macular degeneration is similar to dry macular degeneration, with the build-up of abnormal yellow pigment substance called lipofuscin building up in cells underlying the macula. Patients will also experience problem with night vision, and it will be difficult for them to move around in places with low lighting. In some others, the patient may also experience colour impairment at advanced stages of the disease.
Vision loss is usually slow, until the 20/40 level. It may suddenly shoot right up to 20/200 where the patient is considered legally blind and forbidden from driving. In some cases, it may even deteriorate to 10/200 within a matter of months.
Genes are a big issue when it comes to Stargardt macular degeneration. A group of genes collectively known as the ABC genes, was found to be the culprit of this juvenile macular degeneration, a discovery made since 1997. The ABCA4 gene, responsible for the production of protein used as an energy transport to and from photoreceptor cells in the retina, mutates and produces dysfunctional protein that cannot perform such transport function. The useless ABCA4 protein then allows the accumulation of yellow, fatty material to accumulate in the retina, slowly covering the macularand ultimately causes the loss of vision. However, more studies had to be done to further understand how the mutated genes affect the biochemistry of the retina.
All is not lost for patients with Stargardt disease. It was found that patients may slow down the progression of vision loss by wearing UV protective sunglasses and avoid exposure to bright light. Although there is not yet any effective treatment for this form of macular degeneration at this moment, it is believed that the identification of the genes behind macular degeneration will help the search for new strategies and therapies. The latest is a study scheduled to begin in 2011, for the injection of embryonic stem cells into the eyes of twelve patients affected by the disease. The Advanced Cell Technology announced in November 2010 that the FDA had approved this injection and study.
Stargardt Macular Degeneration may be either autosomal or recessive trait type. A person may not have prior family history, but may have a recessive gene. If both parents carry a mutated gene, there is always a chance for the child to develop macular dystrophy. In fact, there may be more than one family member who gets Stargardt. For children who did not develop Stargardt, there is again the possibility of carrying the mutant gene, and pass on to their children instead. The chances will be 25%.
Three tests are used to check the presence of fundus flecks and the loss of cones to determine whether a patient has Stargardt Macular Degeneration. It may be fluorescein angiography, electroretinography or electrooculography. Since this problem is rare, it is not a widely studied subject. The discovery of genetic mutation in Stargardt may have encouraged the findings of genetic links for age-related macular degeneration, but further studies on the age-related macular degeneration may also become the contributing factor towards better understanding of Stargardt’s disease and its possible lead to new treatment. Whichever way it may be, it will always remain hopeful for parents and their affected children.
Saturday, January 15, 2011
Can Eye Drops With Pirenoxine Be Used to Treat Cataracts?
by;Dr. Ari Weitzner
For over 60 years, cataracts has been treated in China with eye drops containing the non-prescription drug pirenoxine.
Researchers recently tested the potential effectiveness of pirenoxine as a treatment for cataracts by investigating whether and how pirenoxine interacts with selenite or calcium ions, which have been proven as factors leading to the formation of lens cataracts.
As reported in the journal Inorganic Chemistry, researchers found that pirenoxine reduced the cloudiness of the lens solution containing calcium by 38 per cent and reduced the cloudiness of the selenite solution by 11 per cent.
Researchers concluded that the results may provide a rationale for using pirenoxine as an anti-cataract agent and advocated further biological studies.
For over 60 years, cataracts has been treated in China with eye drops containing the non-prescription drug pirenoxine.
Researchers recently tested the potential effectiveness of pirenoxine as a treatment for cataracts by investigating whether and how pirenoxine interacts with selenite or calcium ions, which have been proven as factors leading to the formation of lens cataracts.
As reported in the journal Inorganic Chemistry, researchers found that pirenoxine reduced the cloudiness of the lens solution containing calcium by 38 per cent and reduced the cloudiness of the selenite solution by 11 per cent.
Researchers concluded that the results may provide a rationale for using pirenoxine as an anti-cataract agent and advocated further biological studies.
Sunday, January 9, 2011
Novartis gains new indication for Lucentis in EU for vision loss due to Diabetic Macular Edema
By:Financial
The European Commission has granted Novartis a new indication for Lucentis (ranibizumab) to treat patients with visual impairment due to diabetic macular edema (DME), a leading cause of blindness in the working-age population in most developed countries.
Laser therapy, the current standard of care, has provided stabilization of vision in many patients, but generally does not improve vision. Lucentis is the first licensed therapy to significantly improve both vision and vision-related quality of life in patients with visual impairment due to DME.
"Similarly to wet age related macular degeneration, diabetic macular edema can cause disabling vision loss. While vision loss as a consequence of diabetes affects only a very small proportion of people with the disease, it is one of the most feared complications," said Don Curran, Chair, AMD Alliance International. "Visual impairment impacts everything from managing social interactions to the ability to work - thus, for most people it means a loss of independence."
The approval of Lucentis was based on data from two Novartis-sponsored clinical trials, RESTORE and RESOLVE, which showed that Lucentis was superior in providing rapid and sustained visual acuity gain versus sham (dummy) therapy or laser therapy, the current standard of care.
"In the clinical trials, Lucentis-treated patients began to recover their vision as early as eight days after the first injection on average, and vision improvement was maintained at one year," said Gabriele E. Lang, Professor, University Eye Hospital, University of Ulm, Germany. "The vision improvement for many of these patients was clinically significant, meaning that they regained the ability to carry out day-to-day activities such as driving."
The RESTORE study showed patients treated with Lucentis alone or with Lucentis plus laser therapy gained an average of 6.8 letters and 6.4 letters, respectively, in visual acuity at 12 months compared to baseline, while laser-treated patients gained an average of 0.9 letters as measured on a standard ETDRS eye chart.
The RESOLVE study showed that Lucentis-treated patients gained an average of 10.3 letters in visual acuity at 12 months compared to baseline while sham-treated patients, some of whom also received laser treatment, lost an average of 1.4 letters.
"Since its first launch in the EU in 2007, Lucentis has become the gold standard treatment of wet AMD and its use has stimulated research into other ocular conditions," said David Epstein, Division Head of Novartis Pharmaceuticals. "Our continued investment in the clinical development of Lucentis means that another group of patients who are at risk of losing their eyesight will have the option of a licensed therapy that could help save their vision."
"The pivotal data from RESTORE and RESOLVE studies are further supported by results of an independent US study examining Lucentis for the treatment of DME compared to standard of care. Conducted by the Diabetic Retinopathy Clinical Research Network (DRCR.net), this study showed that at 12 months patients treated with Lucentis plus laser gained an average of nine letters in visual acuity compared to baseline while patients treated with laser therapy alone gained an average of three to four letters. In addition, the study demonstrated superior gains in visual acuity among Lucentis-treated patients up to two years, with a reduced number of Lucentis injections required the second year compared to the first. Specifically, there was a median of only two to three injections required in the second year of treatment compared to a median of eight to nine injections required in the first year," Novartis said.
Diabetic macular edema (DME) is a consequence of diabetic retinopathy, the most common diabetic eye complication. DME is characterized by changes in the blood vessels of the retina, which is the light-sensitive layer at the back of the eye. In patients with DME, leakage from these abnormal blood vessels occurs in the central portion of the retina, called the macula. Because this part of the eye is responsible for sharp central vision, DME can lead to significant visual impairment. Visual impairment due to DME affects approximately 1-3% of patients with diabetes, and DME is a leading cause of blindness in the working-age population in most developed countries.
Lucentis offers an entirely new pharmacological approach to treatment for visual impairment due to DME compared to the current standard of care, which involves the use of laser burns to stop capillary leakage and reduce swelling. Lucentis is an antibody fragment that is injected into the eye and neutralizes vascular endothelial growth factor (VEGF), a protein that is known to increase vascular permeability, resulting in capillary leakage and macular edema in patients with diabetes.
Lucentis was generally well tolerated in DME clinical studies, either when given as monotherapy or when combined with laser treatment. Its safety profile was consistent with the well established profile in patients with wet age-related macular degeneration (wet AMD). There was an incidence of arterial thromboembolic events (<=3.5%) observed in the DME clinical trials, consistent with what was seen in the wet AMD clinical trials, with no significant difference between the groups treated with Lucentis compared to sham or laser therapy. Ocular adverse events were similar to those seen in the wet AMD trials, with an incidence of 1.4% endophthalmitis in the pooled pivotal studies.
Lucentis is currently licensed in more than 85 countries for the treatment of wet AMD. It receives continuous safety monitoring via a systematic pharmacovigilance system and there is more than 750,000 patient-treatment years of exposure to date for Lucentis.
Lucentis was developed by Genentech and Novartis. Genentech has the commercial rights to Lucentis in the United States, where Lucentis is also approved for the treatment of macular edema following retinal vein occlusion (RVO). In addition, Genentech is conducting two Phase III studies, RISE and RIDE, in patients with diabetic macular edema with results expected in 2011. Novartis has exclusive rights in the rest of the world and has filed in the European Union for approval of Lucentis for the treatment of visual impairment due to macular edema secondary to RVO.
The European Commission has granted Novartis a new indication for Lucentis (ranibizumab) to treat patients with visual impairment due to diabetic macular edema (DME), a leading cause of blindness in the working-age population in most developed countries.
Laser therapy, the current standard of care, has provided stabilization of vision in many patients, but generally does not improve vision. Lucentis is the first licensed therapy to significantly improve both vision and vision-related quality of life in patients with visual impairment due to DME.
"Similarly to wet age related macular degeneration, diabetic macular edema can cause disabling vision loss. While vision loss as a consequence of diabetes affects only a very small proportion of people with the disease, it is one of the most feared complications," said Don Curran, Chair, AMD Alliance International. "Visual impairment impacts everything from managing social interactions to the ability to work - thus, for most people it means a loss of independence."
The approval of Lucentis was based on data from two Novartis-sponsored clinical trials, RESTORE and RESOLVE, which showed that Lucentis was superior in providing rapid and sustained visual acuity gain versus sham (dummy) therapy or laser therapy, the current standard of care.
"In the clinical trials, Lucentis-treated patients began to recover their vision as early as eight days after the first injection on average, and vision improvement was maintained at one year," said Gabriele E. Lang, Professor, University Eye Hospital, University of Ulm, Germany. "The vision improvement for many of these patients was clinically significant, meaning that they regained the ability to carry out day-to-day activities such as driving."
The RESTORE study showed patients treated with Lucentis alone or with Lucentis plus laser therapy gained an average of 6.8 letters and 6.4 letters, respectively, in visual acuity at 12 months compared to baseline, while laser-treated patients gained an average of 0.9 letters as measured on a standard ETDRS eye chart.
The RESOLVE study showed that Lucentis-treated patients gained an average of 10.3 letters in visual acuity at 12 months compared to baseline while sham-treated patients, some of whom also received laser treatment, lost an average of 1.4 letters.
"Since its first launch in the EU in 2007, Lucentis has become the gold standard treatment of wet AMD and its use has stimulated research into other ocular conditions," said David Epstein, Division Head of Novartis Pharmaceuticals. "Our continued investment in the clinical development of Lucentis means that another group of patients who are at risk of losing their eyesight will have the option of a licensed therapy that could help save their vision."
"The pivotal data from RESTORE and RESOLVE studies are further supported by results of an independent US study examining Lucentis for the treatment of DME compared to standard of care. Conducted by the Diabetic Retinopathy Clinical Research Network (DRCR.net), this study showed that at 12 months patients treated with Lucentis plus laser gained an average of nine letters in visual acuity compared to baseline while patients treated with laser therapy alone gained an average of three to four letters. In addition, the study demonstrated superior gains in visual acuity among Lucentis-treated patients up to two years, with a reduced number of Lucentis injections required the second year compared to the first. Specifically, there was a median of only two to three injections required in the second year of treatment compared to a median of eight to nine injections required in the first year," Novartis said.
Diabetic macular edema (DME) is a consequence of diabetic retinopathy, the most common diabetic eye complication. DME is characterized by changes in the blood vessels of the retina, which is the light-sensitive layer at the back of the eye. In patients with DME, leakage from these abnormal blood vessels occurs in the central portion of the retina, called the macula. Because this part of the eye is responsible for sharp central vision, DME can lead to significant visual impairment. Visual impairment due to DME affects approximately 1-3% of patients with diabetes, and DME is a leading cause of blindness in the working-age population in most developed countries.
Lucentis offers an entirely new pharmacological approach to treatment for visual impairment due to DME compared to the current standard of care, which involves the use of laser burns to stop capillary leakage and reduce swelling. Lucentis is an antibody fragment that is injected into the eye and neutralizes vascular endothelial growth factor (VEGF), a protein that is known to increase vascular permeability, resulting in capillary leakage and macular edema in patients with diabetes.
Lucentis was generally well tolerated in DME clinical studies, either when given as monotherapy or when combined with laser treatment. Its safety profile was consistent with the well established profile in patients with wet age-related macular degeneration (wet AMD). There was an incidence of arterial thromboembolic events (<=3.5%) observed in the DME clinical trials, consistent with what was seen in the wet AMD clinical trials, with no significant difference between the groups treated with Lucentis compared to sham or laser therapy. Ocular adverse events were similar to those seen in the wet AMD trials, with an incidence of 1.4% endophthalmitis in the pooled pivotal studies.
Lucentis is currently licensed in more than 85 countries for the treatment of wet AMD. It receives continuous safety monitoring via a systematic pharmacovigilance system and there is more than 750,000 patient-treatment years of exposure to date for Lucentis.
Lucentis was developed by Genentech and Novartis. Genentech has the commercial rights to Lucentis in the United States, where Lucentis is also approved for the treatment of macular edema following retinal vein occlusion (RVO). In addition, Genentech is conducting two Phase III studies, RISE and RIDE, in patients with diabetic macular edema with results expected in 2011. Novartis has exclusive rights in the rest of the world and has filed in the European Union for approval of Lucentis for the treatment of visual impairment due to macular edema secondary to RVO.
Sunday, January 2, 2011
Macular Degeneration Treatments
by:Akler Eye Center
Macular degeneration, or Age-Related Macular Degeneration (ARMD) is a condition related to aging of the eye that causes loss of the central vision. It is the commonest cause of blindness in Americans over 55 years old. Approximately 10 million people in the United States are affected. Smoking, high blood pressure, family history of ARMD, and poor diet are all risk factors for the development of ARMD.
The macula is the center most part of the retina, and is responsible for the sharp vision that allows us to read and drive. In some people, as the eye ages, deposits develop in the retina (dry ARMD). This can cause the macula to function imperfectly, which leads to blurry vision. Only 10% of patients develop the wet form of ARMD. In this more devastating form, abnormal blood vessels grow in the macula, and when they leak or bleed, severe loss of the central vision often results.
The symptoms of macular degeneration are blurring of the vision, which causes difficulty with reading or driving. Macular degeneration does not cause total blindness because the side vision is not affected.
At Akler Eye Center in Dearborn MI, a complete eye examination including dilation of the pupil will allow Dr. Akler to detect both mild and severe forms of macular degeneration. If ARMD is found, further testing may include a fluorescein angiogram and optical coherence tomography (OCT). Fluorescein angiography involves injecting dye into the arm and photographing it as it circulates in the retina. Abnormal blood vessel growth and leakage may be detected. OCT is a computerized picture of the macula that shows if it is swollen with fluid. Both of these tests are performed onsite.
Treatments for macular degeneration are primarily targeted at keeping the retina as healthy as possible and screening for early signs of the wet form of ARMD. A study performed by the National Eye Institute demonstrated that taking special vitamins for the eye that contain anti-oxidants (A, C, E and beta-carotene with zinc) reduces the risk of developing severe vision loss. A home screening tool known as an Amsler Grid allows the patient to check the vision with one eye at a time. If the grid paper lines are wavy or faded, an eye examination is needed urgently.
If the wet form of ARMD is present, the current treatment involves injection of medication into the eye. The medication is targeted at reducing the growth of abnormal blood vessels in the macula.
Dr. Michelle Akler recommends regular eye examinations to screen for macular degeneration, especially in older patients and those with a family history of ARMD. Early detection and treatment allows for the best visual outcome in this difficult condition.
Macular degeneration, or Age-Related Macular Degeneration (ARMD) is a condition related to aging of the eye that causes loss of the central vision. It is the commonest cause of blindness in Americans over 55 years old. Approximately 10 million people in the United States are affected. Smoking, high blood pressure, family history of ARMD, and poor diet are all risk factors for the development of ARMD.
The macula is the center most part of the retina, and is responsible for the sharp vision that allows us to read and drive. In some people, as the eye ages, deposits develop in the retina (dry ARMD). This can cause the macula to function imperfectly, which leads to blurry vision. Only 10% of patients develop the wet form of ARMD. In this more devastating form, abnormal blood vessels grow in the macula, and when they leak or bleed, severe loss of the central vision often results.
The symptoms of macular degeneration are blurring of the vision, which causes difficulty with reading or driving. Macular degeneration does not cause total blindness because the side vision is not affected.
At Akler Eye Center in Dearborn MI, a complete eye examination including dilation of the pupil will allow Dr. Akler to detect both mild and severe forms of macular degeneration. If ARMD is found, further testing may include a fluorescein angiogram and optical coherence tomography (OCT). Fluorescein angiography involves injecting dye into the arm and photographing it as it circulates in the retina. Abnormal blood vessel growth and leakage may be detected. OCT is a computerized picture of the macula that shows if it is swollen with fluid. Both of these tests are performed onsite.
Treatments for macular degeneration are primarily targeted at keeping the retina as healthy as possible and screening for early signs of the wet form of ARMD. A study performed by the National Eye Institute demonstrated that taking special vitamins for the eye that contain anti-oxidants (A, C, E and beta-carotene with zinc) reduces the risk of developing severe vision loss. A home screening tool known as an Amsler Grid allows the patient to check the vision with one eye at a time. If the grid paper lines are wavy or faded, an eye examination is needed urgently.
If the wet form of ARMD is present, the current treatment involves injection of medication into the eye. The medication is targeted at reducing the growth of abnormal blood vessels in the macula.
Dr. Michelle Akler recommends regular eye examinations to screen for macular degeneration, especially in older patients and those with a family history of ARMD. Early detection and treatment allows for the best visual outcome in this difficult condition.
Monday, December 27, 2010
Treatment For Wet Macular Degeneration in Seniors
by: Admin
The National Eye Institute (NEI) had published their facts about Age-Related Macular Degeneration (ARMD) to help patients and their family members to search for general information about the disease.
Age Related Wet Macular Degeneration
In its attempt to ensure better public understanding of the disease, it had detailed the ARMD by starting on its definition. The NEI defined ARMD as “a disease associated with aging that gradually destroys sharp, central vision.” It is then explained that central vision is important to see fine details and helps common daily tasks such as reading and driving. It has to be noted that ARMD causes no physical pain to the patients.
There are two types of ARMD, which is the dry and the wet ARMD. In most cases, elderly adults develop the dry ARMD and it is the most common form of the disease, with some of them progressing into wet ARMD when abnormal blood vessels start developing and ruptures within. Wet ARMD can be treated, but not fully cured, by laser surgery, photodynamic therapy and injections into the eye. These treatments may actually just delay the process of being legally blind, but patients need to be aware that conditions will continue to worsen over time.
Treating wet ARMD with Laser surgery is a procedure which utilizes the laser technology to destroy fragile, leaky blood vessels that had formed abnormally. A high energy light beam is directly focused on the new blood vessels, and it destroys them to prevent further loss of vision. The negative side of this treatment is that it potentially destroys other healthy cells surrounding the treatment area.
Only a small percentage of patients may use laser to treat wet ARMD. The procedure is performed at the doctor’s office or an eye clinic, and laser is more effective if the abnormal, leaky blood vessels are developed away from the middle of the macula, which is called the fovea. It does not mean that the abnormal blood vessels will automatically stop developing after laser surgery, in fact repeated treatments are necessary as the risk of developing new abnormal blood vessels post surgery is high. In some cases, the patient may still suffer vision loss progressively despite repeated treatments.
Another treatment, called the photodynamic therapy, involves the injection of a drug called verteporfin into the patient’s arm, and it travels throughout the body including the new blood vessels in the eye. The drug will attach itself to the surface of new blood vessels. After this, the doctor shines a light into the patients eye for about 90 seconds to activate the drug. The drug, once activated, will destroy the new blood vessels and helps slower down the rate of vision decline. It is topical and aims only at the new blood vessels, so it does not destroy surrounding healthy tissues and cells like the laser surgery.
However, caution has to be taken with the use of this drug. As it gets activated by lights, patient has to avoid going outdoors, or exposing skin or eye to direct sunlight or bright indoor lights for five days after treatment. Remember that the drug is administered through injection on the patient’s arm, and the fact that it travels throughout the body instead of being contained within the eye.
This treatment is basically painless, and can be performed at the doctor’s office in about 20 minutes. However, while it slows down the rate of vision loss, it does not stop vision loss, or restore the patient’s vision if it was already damaged by ARMD. Again, this technique will require repeated treatments as necessary, based on the doctor’s prescription and the progress of your condition.
Another treatment is the use of injection, this time with new drugs that are injected directly into the eyes. The anti-VEGF therapy will see these new drugs block the effects of the specific growth factor that triggers the abnormal blood vessels. Multiple injections will be required, and it can be a monthly affair. Before injection, the eyes are numbed. After injection, the patient will be kept at the doctor’s office for a while so that the doctor may monitor the progress of the eyes before declaring that the patient is safe to go home. It is said that this treatment helps slow down vision loss from ARMD and may also help to improve the sight of patients in some cases.
In any of these treatments, the patient should listen to the doctor because the doctor will know the best option available for each individual.
The National Eye Institute (NEI) had published their facts about Age-Related Macular Degeneration (ARMD) to help patients and their family members to search for general information about the disease.
Age Related Wet Macular Degeneration
In its attempt to ensure better public understanding of the disease, it had detailed the ARMD by starting on its definition. The NEI defined ARMD as “a disease associated with aging that gradually destroys sharp, central vision.” It is then explained that central vision is important to see fine details and helps common daily tasks such as reading and driving. It has to be noted that ARMD causes no physical pain to the patients.
There are two types of ARMD, which is the dry and the wet ARMD. In most cases, elderly adults develop the dry ARMD and it is the most common form of the disease, with some of them progressing into wet ARMD when abnormal blood vessels start developing and ruptures within. Wet ARMD can be treated, but not fully cured, by laser surgery, photodynamic therapy and injections into the eye. These treatments may actually just delay the process of being legally blind, but patients need to be aware that conditions will continue to worsen over time.
Treating wet ARMD with Laser surgery is a procedure which utilizes the laser technology to destroy fragile, leaky blood vessels that had formed abnormally. A high energy light beam is directly focused on the new blood vessels, and it destroys them to prevent further loss of vision. The negative side of this treatment is that it potentially destroys other healthy cells surrounding the treatment area.
Only a small percentage of patients may use laser to treat wet ARMD. The procedure is performed at the doctor’s office or an eye clinic, and laser is more effective if the abnormal, leaky blood vessels are developed away from the middle of the macula, which is called the fovea. It does not mean that the abnormal blood vessels will automatically stop developing after laser surgery, in fact repeated treatments are necessary as the risk of developing new abnormal blood vessels post surgery is high. In some cases, the patient may still suffer vision loss progressively despite repeated treatments.
Another treatment, called the photodynamic therapy, involves the injection of a drug called verteporfin into the patient’s arm, and it travels throughout the body including the new blood vessels in the eye. The drug will attach itself to the surface of new blood vessels. After this, the doctor shines a light into the patients eye for about 90 seconds to activate the drug. The drug, once activated, will destroy the new blood vessels and helps slower down the rate of vision decline. It is topical and aims only at the new blood vessels, so it does not destroy surrounding healthy tissues and cells like the laser surgery.
However, caution has to be taken with the use of this drug. As it gets activated by lights, patient has to avoid going outdoors, or exposing skin or eye to direct sunlight or bright indoor lights for five days after treatment. Remember that the drug is administered through injection on the patient’s arm, and the fact that it travels throughout the body instead of being contained within the eye.
This treatment is basically painless, and can be performed at the doctor’s office in about 20 minutes. However, while it slows down the rate of vision loss, it does not stop vision loss, or restore the patient’s vision if it was already damaged by ARMD. Again, this technique will require repeated treatments as necessary, based on the doctor’s prescription and the progress of your condition.
Another treatment is the use of injection, this time with new drugs that are injected directly into the eyes. The anti-VEGF therapy will see these new drugs block the effects of the specific growth factor that triggers the abnormal blood vessels. Multiple injections will be required, and it can be a monthly affair. Before injection, the eyes are numbed. After injection, the patient will be kept at the doctor’s office for a while so that the doctor may monitor the progress of the eyes before declaring that the patient is safe to go home. It is said that this treatment helps slow down vision loss from ARMD and may also help to improve the sight of patients in some cases.
In any of these treatments, the patient should listen to the doctor because the doctor will know the best option available for each individual.
Monday, December 20, 2010
Zeaxanthin For Macular Degeneration Prevention and Treatment in Dry AMD
by The Pulitzer
Most ophthalmologists recommend the antioxidants lutein and zeaxanthin for macular degeneration that is age related, commonly referred to as AMD. It is unusual for doctor’s to recommend nutritional supplements of any kind, unless a person has an outright deficiency, but AMD is a unique condition.
There are no effective treatments for one type of AMD (dry), but there are some partially effective treatments for wet AMD. Together, these two are the major causes of blindness in the elderly. The wet form is the most severe, if not treated early.
In wet AMD, blood vessels grow up and behind the retina, an area responsible for gathering light and transmitting signals to the brain, resulting in sight. The blood vessels often rupture and leak blood and protein below the macula, a very sensitive area within the retina.
Eventually, bleeding, leaking and scarring causes irreversible damage to the light receptors (rods and cones). Rapid vision loss is experienced if it is left untreated. Laser treatment and drugs that inhibit blood vessel growth are usually recommended.
Generally, doctors recommend lutein and zeaxanthin for macular degeneration that is of the dry type. Dry AMD is much more common than wet. It is caused by a build up of yellow deposits called drusen on the retina.
In nature lutein and zeaxanthin are pigments or colors. They are normally present in the retina, with zeaxanthin being concentrated in the macula and lutein more highly concentrated in the periphery of the retina. There roles within the eye are not well understood, but they seem to help reduce or prevent the build up of drusen.
Drusen is similar in composition to the deposits that are found in the brains of Alzheimer’s patients and the plaque that is present in atherosclerosis. People with either of those two conditions have a higher risk of developing dry AMD.
Some doctors recommend taking lutein and zeaxanthin for macular degeneration prevention, particularly to their patients that have a family history of the disease. But, since the drusen are similar to the deposits that cause Alzheimer’s and heart disease, other antioxidants may be beneficial, as well.
Curcumin, an antioxidant present in the spice turmeric, is currently being studied for its benefit in Alzheimer’s disease. Not only does it prevent the accumulation of the plaque, it breaks it up. It might be able to break up the drusen in AMD, too.
One study indicates that the ideal combination of nutrients is omega 3 fatty acids, beta carotene, vitamin E, lutein and zeaxanthin for macular degeneration. Omega 3 fatty acids, particularly DHA, are the most abundant fatty acids present in the retina. Beta-carotene is converted by the body to vitamin A, which is essential for good vision. Vitamin E is well-known for its antioxidant activity.
Prevention is worth a pound of cure, they say. In order to prevent AMD, people should lower their total fat intake, and increase their nutrient intake. This may help reduce the risk of many other diseases, as well. Taking zeaxanthin for macular degeneration prevention is a good idea. Taking a multi-nutritional supplement that contains it, is a great one.
Valerie Rosenbaum researches omega 3 fish oil supplements, anti aging supplements and natural skincare products. Through her research she has discovered the best anti aging supplement, in both quality and value, available today.
Most ophthalmologists recommend the antioxidants lutein and zeaxanthin for macular degeneration that is age related, commonly referred to as AMD. It is unusual for doctor’s to recommend nutritional supplements of any kind, unless a person has an outright deficiency, but AMD is a unique condition.
There are no effective treatments for one type of AMD (dry), but there are some partially effective treatments for wet AMD. Together, these two are the major causes of blindness in the elderly. The wet form is the most severe, if not treated early.
In wet AMD, blood vessels grow up and behind the retina, an area responsible for gathering light and transmitting signals to the brain, resulting in sight. The blood vessels often rupture and leak blood and protein below the macula, a very sensitive area within the retina.
Eventually, bleeding, leaking and scarring causes irreversible damage to the light receptors (rods and cones). Rapid vision loss is experienced if it is left untreated. Laser treatment and drugs that inhibit blood vessel growth are usually recommended.
Generally, doctors recommend lutein and zeaxanthin for macular degeneration that is of the dry type. Dry AMD is much more common than wet. It is caused by a build up of yellow deposits called drusen on the retina.
In nature lutein and zeaxanthin are pigments or colors. They are normally present in the retina, with zeaxanthin being concentrated in the macula and lutein more highly concentrated in the periphery of the retina. There roles within the eye are not well understood, but they seem to help reduce or prevent the build up of drusen.
Drusen is similar in composition to the deposits that are found in the brains of Alzheimer’s patients and the plaque that is present in atherosclerosis. People with either of those two conditions have a higher risk of developing dry AMD.
Some doctors recommend taking lutein and zeaxanthin for macular degeneration prevention, particularly to their patients that have a family history of the disease. But, since the drusen are similar to the deposits that cause Alzheimer’s and heart disease, other antioxidants may be beneficial, as well.
Curcumin, an antioxidant present in the spice turmeric, is currently being studied for its benefit in Alzheimer’s disease. Not only does it prevent the accumulation of the plaque, it breaks it up. It might be able to break up the drusen in AMD, too.
One study indicates that the ideal combination of nutrients is omega 3 fatty acids, beta carotene, vitamin E, lutein and zeaxanthin for macular degeneration. Omega 3 fatty acids, particularly DHA, are the most abundant fatty acids present in the retina. Beta-carotene is converted by the body to vitamin A, which is essential for good vision. Vitamin E is well-known for its antioxidant activity.
Prevention is worth a pound of cure, they say. In order to prevent AMD, people should lower their total fat intake, and increase their nutrient intake. This may help reduce the risk of many other diseases, as well. Taking zeaxanthin for macular degeneration prevention is a good idea. Taking a multi-nutritional supplement that contains it, is a great one.
Valerie Rosenbaum researches omega 3 fish oil supplements, anti aging supplements and natural skincare products. Through her research she has discovered the best anti aging supplement, in both quality and value, available today.
Saturday, December 11, 2010
Advance Cell Technology's CEO says Markets Are Just Starting to Appreciate the Significance of Thei
by Advance Cell Technology
The excitement around ACTC comes after a recent series of key positive announcements including the fact that the FDA granted orphan drug status to the micro-cap's patented embryonic stem cell derived treatment for specific forms of Macular Degeneration and blindness (Stargardt's Macular Dystrophy and Dry Age-related Macular Degeneration). The eye conditions destroy the pigmented layer of retina (retinal pigment epithelium) which is the pigmented cell layer just outside the neurosensory retina that nourishes retinal visual cells.
The condition destroys the pigmented layer of retina (retinal pigment epithelium) which is the pigmented cell layer just outside the neurosensory retina that nourishes retinal visual cells. Advanced Cell Technology has shown success introducing the embryonic stem cell derived RPE cells into the eye in animal models and this resulted in 100% improvement with no side effects for more than 220 days. Human clinical trials are expected to start in the first quarter of 2011, and can potentially take only a few weeks to show positive results.
Advanced Cell Technology has shown success introducing the embryonic stem cell derived RPE cells into the eye in animal models and this resulted in 100% improvement with no side effects for more than 220 days. Human clinical trials are expected to start in the first quarter of 2011, and could potentially take only a few weeks to show positive results according to some analysts.
In addition, for only the second time in history (following Geron's therapy for spinal cord injury), the FDA granted approval for clinical trials for a therapy derived from human embryonic stem cells.
William M. Caldwell, Chairman and CEO of ACTC tells BioMedReports that ACTC plans on building upon their orphan drug status and accelerating clinical testing. In addition, they hope to continue showing promising advancements in other forms of regenerative medicine which the company is developing -- most notably its Myoblast program for the treatment of heart failure. The Myoblast program (part of the company's 2007 acquisition of Mytogen, Inc.) has successfully completed Phase I human clinical trials and the FDA has finished reviewing the data, thus allowing Advanced Cell Technology to proceed with a Phase II human clinical trial (in approximately 160 patients) early next year.
BioMedReports: It appears that suddenly your company has a lot of attention given your news developments. What do you make of all the activity in your stock during recent days?
William M. Caldwell, Chairman and CEO of ACTC: The market is starting to appreciate the significance of the FDA approval of our particular therapy. I think they are now beginning to understand the strategy of having filed for an orphan indication designation for Stargardt's Macular Dystrophy (SMD is one of the most common forms of juvenile macular degeneration in the world) and they now realize that that represents the first wave, with potentially huge commercial opportunities in Dry AMD (Dry Age-Related Macular Degeneration reportedly afflicts more than 30 million people worldwide, including an estimated 13-15 million Americans). Both indications do not have viable therapies and so to the extent that our program can make an impact, it's going to not only help a very large patient population, it -- as well as any other therapies that are approved -- will help validate a very large technology.
BioMedReports: Can you help us digest or simplify what some of those implications are?
William M. Caldwell, Chairman and CEO of ACTC: I can certainly try. Right now, Genentech has a drug on the market for Wet AMD [Note: the FDA approved Lucentis in 2006 after a 6-month priority review] and that patient population is substantially less than the Dry AMD component. Their procedure is to apply a needle into the eye every two to three months with their therapy and for that they get some $2500, plus or minus, for each injection. In our particular situation, we are inserting a needle into the eye- which is something that is done all the time, by the way, this isn't something that's foreign to the practitioner that does the application -- but our application takes place only once or possibly twice over the life of the patient. It is our expectation that the therapy which we'll apply will have an impact on either slowing down or arresting the progression of the disease. We've seen that in our animal models. There have been some very dramatic results when we've applied it into animals and we are extremely hopeful that we will see the same types of results when we apply it into humans.
The problem has been that this technology is totally new to the world of medicine. It is an embryonic stem cell derived therapy. It turns out that our cells have been derived utilizing what we call a blastomere technology which means that we have been able to develop those stem cells without any embryo destruction, which somewhat mitigates the issues that have been in the media.
So, we take our particular stem cell therapy -- and remember that the stem cells are converted into a single cell type so there's really no actual stem cells into the therapy that we are applying only a certain cell-type and in this particular case, it's what they call RPE (retinal pigment epithelial) cells. That RPE layer is in the eye between the photoreceptor and the Bruch's membrane. It protects that photoreceptor -- which gives us the ability to see -- and it also nourishes it. With deterioration, all sorts of different diseases occur. One of which is Stargardt's Macular Dystrophy and another of which is Dry AMD. Now, there are certainly different characteristics to those, but to the extent that you can replenish that RPE layer with new, healthy, viable cells you have the opportunity to dramatically impact the deterioration that is occurring within the photoreceptor.
That's a layman's description of what we're doing with respect to that therapy, but more importantly the market implication is such that if you have in excess of ten million patients currently suffering from that disease; which is age related and as we know the baby boomers are getting older. Unfortunately for those of us that are getting into that post fifty-five or sixty year-old age range, those individuals are prime candidates for this disease. That market is fairly significant. There is an opportunity of tremendous magnitude for a company like ours.
BioMedReports: Let's talk about the structure of the company for a bit. There have been some concerns that there are a lot of shares out there and that a company that is set up in this way could suddenly announce something like a reverse-split during a run-up in price like this one. What are your comments in regard to that as far as ACTC goes?
William M. Caldwell, Chairman and CEO of ACTC: I'm an investment banker and I can tell you that it has been my experience that reverse splits for the sake of reverse splits are very problematic. There has to be a rationale behind why someone would do such a thing and it has to be done around some sort of event that is accretive to shareholders and makes logical sense for all the stakeholders. I'm not inclined at all to recommend a reverse split unless that opportunity presented itself. If it does, based upon our charter, we would then have to go to the shareholders for their approval. In that way they would have an opportunity to understand our rationale and determine whether that makes sense for the majority of them. I think that's about all I can say about that subject at this stage.
BioMedReports: Can you talk about any of the upcoming milestones for the company? Some think that is part of the reason for this run-up, that there are some events worth looking forward to on the horizon.
William M. Caldwell, Chairman and CEO of ACTC: I think we've alluded to some things a couple of times either on blogs or in conferences, and I can start with the approval of our IND for Stargardt's Disease which we will be seeing some time in the first half of the coming year. (That will mark) us going into the clinic. And we have already alluded to the fact that we will go into multiple sites, not just one particular site, for the reason that we have filed for Phase I/Phase II. For those who are not familiar with that, Phase I really focuses on safety. That's going to be a very, very important piece, not just because of the safety, but because it will ensure for the FDA that this cell type can be safe in humans.
You know the first one is always the toughest one, so we've designed the trial to be very, very slow in its evolution. We have a dosage escalation schedule whereby we're only inserting a minimal amount of cells at the outset per patient. Then we will increase that with ensuing patients and we'll pause to allow the FDA to review the results of that so that they can feel comfortable with the safety issues related to the fact that the cells go where they are supposed to go and do what they're supposed to do and that they don't cause any side effects, or tumors or anything else that has been ballyhooed around. By the way, we have never, in any of our studies, ever seen that.
So, I can't speak for others, but for us; our patented differentiation processes are such that our cells are terminally and totally differentiated into the cell type that we're dealing with. Once we do that, then we'll move quickly into efficacy and that tells us, of course, "does it work?" And that's why we're starting out with multiple sites. Right now, I'm in the process of finalizing those sites and developing a relationship with the primary investigator -- the surgeon at each of the sites. I'm working with the internal review boards to gain approval on the protocols on any specific issues that they may have relative to their particular situation and then we will initiate those trials when all of that is completed.
The second major milestone is that we've filed a second IND. That one is for the Dry AMD and we anticipate that it will take much less time for the FDA to evaluate that, versus the time they took to evaluate the first one. We anticipate that sometime in the first quarter (of 2011) there is a very reasonable chance that we will see approval for that IND -- at which time we will then initiate trials for that program as well. Just so you know, it's the same cells. So we're really just taking the same cell-type and treating a different disease-type. So that's why we're relatively bullish on that particular program.
A third area that we've announced is that as big as the market is, and the opportunity is here in the United States, the European community offers a similar opportunity. And with the E.U. controlling the regulatory perspective for the various countries on the continent, we will be looking very hard at the opportunity to take both our Stargardt's and Dry AMD programs over there. I've been spending some time over there trying to ascertain what the best way is to do it and where the best places are to initiate the trials as well as learning a little bit about the process of how to work through the regulatory situations over there. We should be in position to make an announcement about that in the first half of next year.
We've also mentioned another disease condition called our Myoblast or heart program. It's an adult stem cell -- meaning it's the patient's own cells -- in this particular instance. We extract out of the thigh in a biopsy and then we re-place it into the heart with a catheter system. Basically, it goes over the dead heart tissue from a heart attack that a patient has had. And what those cells do, those myoblast cells, is they integrate with the good cardio myocyte cells -- the heart cells -- and help those cells pump the blood in and out of the heart. That's important because when you have a heart attack, part of your heart muscle is killed or dead, and unlike other parts of the body the muscle doesn't regenerate itself and so the remaining muscle has to work harder and the heart becomes a little weaker. Because of the strain on the muscle it gets, sometimes, enlarged. The walls get thinner and that's when you start seeing heart failure. What this does is that it helps mitigate that and the patient can start feeling better. That's really where the FDA is focused on, is the quality of life of the patient. Most of the patients that we're dealing with are in advanced age heart failure. So that is another disease condition. We have gotten approval from the FDA to move out of the Phase I, where we did four trials, and we're moving into Phase II. I've made an announcement that we intend to do that in the first half of next year. So again, that is another program that you should be hearing some things from us about during the first half of next year.
So just in the first half of the coming year we have some fairly significant milestones that we have before us and then there are a couple that we're working on now that we haven't announced yet.
The excitement around ACTC comes after a recent series of key positive announcements including the fact that the FDA granted orphan drug status to the micro-cap's patented embryonic stem cell derived treatment for specific forms of Macular Degeneration and blindness (Stargardt's Macular Dystrophy and Dry Age-related Macular Degeneration). The eye conditions destroy the pigmented layer of retina (retinal pigment epithelium) which is the pigmented cell layer just outside the neurosensory retina that nourishes retinal visual cells.
The condition destroys the pigmented layer of retina (retinal pigment epithelium) which is the pigmented cell layer just outside the neurosensory retina that nourishes retinal visual cells. Advanced Cell Technology has shown success introducing the embryonic stem cell derived RPE cells into the eye in animal models and this resulted in 100% improvement with no side effects for more than 220 days. Human clinical trials are expected to start in the first quarter of 2011, and can potentially take only a few weeks to show positive results.
Advanced Cell Technology has shown success introducing the embryonic stem cell derived RPE cells into the eye in animal models and this resulted in 100% improvement with no side effects for more than 220 days. Human clinical trials are expected to start in the first quarter of 2011, and could potentially take only a few weeks to show positive results according to some analysts.
In addition, for only the second time in history (following Geron's therapy for spinal cord injury), the FDA granted approval for clinical trials for a therapy derived from human embryonic stem cells.
William M. Caldwell, Chairman and CEO of ACTC tells BioMedReports that ACTC plans on building upon their orphan drug status and accelerating clinical testing. In addition, they hope to continue showing promising advancements in other forms of regenerative medicine which the company is developing -- most notably its Myoblast program for the treatment of heart failure. The Myoblast program (part of the company's 2007 acquisition of Mytogen, Inc.) has successfully completed Phase I human clinical trials and the FDA has finished reviewing the data, thus allowing Advanced Cell Technology to proceed with a Phase II human clinical trial (in approximately 160 patients) early next year.
BioMedReports: It appears that suddenly your company has a lot of attention given your news developments. What do you make of all the activity in your stock during recent days?
William M. Caldwell, Chairman and CEO of ACTC: The market is starting to appreciate the significance of the FDA approval of our particular therapy. I think they are now beginning to understand the strategy of having filed for an orphan indication designation for Stargardt's Macular Dystrophy (SMD is one of the most common forms of juvenile macular degeneration in the world) and they now realize that that represents the first wave, with potentially huge commercial opportunities in Dry AMD (Dry Age-Related Macular Degeneration reportedly afflicts more than 30 million people worldwide, including an estimated 13-15 million Americans). Both indications do not have viable therapies and so to the extent that our program can make an impact, it's going to not only help a very large patient population, it -- as well as any other therapies that are approved -- will help validate a very large technology.
BioMedReports: Can you help us digest or simplify what some of those implications are?
William M. Caldwell, Chairman and CEO of ACTC: I can certainly try. Right now, Genentech has a drug on the market for Wet AMD [Note: the FDA approved Lucentis in 2006 after a 6-month priority review] and that patient population is substantially less than the Dry AMD component. Their procedure is to apply a needle into the eye every two to three months with their therapy and for that they get some $2500, plus or minus, for each injection. In our particular situation, we are inserting a needle into the eye- which is something that is done all the time, by the way, this isn't something that's foreign to the practitioner that does the application -- but our application takes place only once or possibly twice over the life of the patient. It is our expectation that the therapy which we'll apply will have an impact on either slowing down or arresting the progression of the disease. We've seen that in our animal models. There have been some very dramatic results when we've applied it into animals and we are extremely hopeful that we will see the same types of results when we apply it into humans.
The problem has been that this technology is totally new to the world of medicine. It is an embryonic stem cell derived therapy. It turns out that our cells have been derived utilizing what we call a blastomere technology which means that we have been able to develop those stem cells without any embryo destruction, which somewhat mitigates the issues that have been in the media.
So, we take our particular stem cell therapy -- and remember that the stem cells are converted into a single cell type so there's really no actual stem cells into the therapy that we are applying only a certain cell-type and in this particular case, it's what they call RPE (retinal pigment epithelial) cells. That RPE layer is in the eye between the photoreceptor and the Bruch's membrane. It protects that photoreceptor -- which gives us the ability to see -- and it also nourishes it. With deterioration, all sorts of different diseases occur. One of which is Stargardt's Macular Dystrophy and another of which is Dry AMD. Now, there are certainly different characteristics to those, but to the extent that you can replenish that RPE layer with new, healthy, viable cells you have the opportunity to dramatically impact the deterioration that is occurring within the photoreceptor.
That's a layman's description of what we're doing with respect to that therapy, but more importantly the market implication is such that if you have in excess of ten million patients currently suffering from that disease; which is age related and as we know the baby boomers are getting older. Unfortunately for those of us that are getting into that post fifty-five or sixty year-old age range, those individuals are prime candidates for this disease. That market is fairly significant. There is an opportunity of tremendous magnitude for a company like ours.
BioMedReports: Let's talk about the structure of the company for a bit. There have been some concerns that there are a lot of shares out there and that a company that is set up in this way could suddenly announce something like a reverse-split during a run-up in price like this one. What are your comments in regard to that as far as ACTC goes?
William M. Caldwell, Chairman and CEO of ACTC: I'm an investment banker and I can tell you that it has been my experience that reverse splits for the sake of reverse splits are very problematic. There has to be a rationale behind why someone would do such a thing and it has to be done around some sort of event that is accretive to shareholders and makes logical sense for all the stakeholders. I'm not inclined at all to recommend a reverse split unless that opportunity presented itself. If it does, based upon our charter, we would then have to go to the shareholders for their approval. In that way they would have an opportunity to understand our rationale and determine whether that makes sense for the majority of them. I think that's about all I can say about that subject at this stage.
BioMedReports: Can you talk about any of the upcoming milestones for the company? Some think that is part of the reason for this run-up, that there are some events worth looking forward to on the horizon.
William M. Caldwell, Chairman and CEO of ACTC: I think we've alluded to some things a couple of times either on blogs or in conferences, and I can start with the approval of our IND for Stargardt's Disease which we will be seeing some time in the first half of the coming year. (That will mark) us going into the clinic. And we have already alluded to the fact that we will go into multiple sites, not just one particular site, for the reason that we have filed for Phase I/Phase II. For those who are not familiar with that, Phase I really focuses on safety. That's going to be a very, very important piece, not just because of the safety, but because it will ensure for the FDA that this cell type can be safe in humans.
You know the first one is always the toughest one, so we've designed the trial to be very, very slow in its evolution. We have a dosage escalation schedule whereby we're only inserting a minimal amount of cells at the outset per patient. Then we will increase that with ensuing patients and we'll pause to allow the FDA to review the results of that so that they can feel comfortable with the safety issues related to the fact that the cells go where they are supposed to go and do what they're supposed to do and that they don't cause any side effects, or tumors or anything else that has been ballyhooed around. By the way, we have never, in any of our studies, ever seen that.
So, I can't speak for others, but for us; our patented differentiation processes are such that our cells are terminally and totally differentiated into the cell type that we're dealing with. Once we do that, then we'll move quickly into efficacy and that tells us, of course, "does it work?" And that's why we're starting out with multiple sites. Right now, I'm in the process of finalizing those sites and developing a relationship with the primary investigator -- the surgeon at each of the sites. I'm working with the internal review boards to gain approval on the protocols on any specific issues that they may have relative to their particular situation and then we will initiate those trials when all of that is completed.
The second major milestone is that we've filed a second IND. That one is for the Dry AMD and we anticipate that it will take much less time for the FDA to evaluate that, versus the time they took to evaluate the first one. We anticipate that sometime in the first quarter (of 2011) there is a very reasonable chance that we will see approval for that IND -- at which time we will then initiate trials for that program as well. Just so you know, it's the same cells. So we're really just taking the same cell-type and treating a different disease-type. So that's why we're relatively bullish on that particular program.
A third area that we've announced is that as big as the market is, and the opportunity is here in the United States, the European community offers a similar opportunity. And with the E.U. controlling the regulatory perspective for the various countries on the continent, we will be looking very hard at the opportunity to take both our Stargardt's and Dry AMD programs over there. I've been spending some time over there trying to ascertain what the best way is to do it and where the best places are to initiate the trials as well as learning a little bit about the process of how to work through the regulatory situations over there. We should be in position to make an announcement about that in the first half of next year.
We've also mentioned another disease condition called our Myoblast or heart program. It's an adult stem cell -- meaning it's the patient's own cells -- in this particular instance. We extract out of the thigh in a biopsy and then we re-place it into the heart with a catheter system. Basically, it goes over the dead heart tissue from a heart attack that a patient has had. And what those cells do, those myoblast cells, is they integrate with the good cardio myocyte cells -- the heart cells -- and help those cells pump the blood in and out of the heart. That's important because when you have a heart attack, part of your heart muscle is killed or dead, and unlike other parts of the body the muscle doesn't regenerate itself and so the remaining muscle has to work harder and the heart becomes a little weaker. Because of the strain on the muscle it gets, sometimes, enlarged. The walls get thinner and that's when you start seeing heart failure. What this does is that it helps mitigate that and the patient can start feeling better. That's really where the FDA is focused on, is the quality of life of the patient. Most of the patients that we're dealing with are in advanced age heart failure. So that is another disease condition. We have gotten approval from the FDA to move out of the Phase I, where we did four trials, and we're moving into Phase II. I've made an announcement that we intend to do that in the first half of next year. So again, that is another program that you should be hearing some things from us about during the first half of next year.
So just in the first half of the coming year we have some fairly significant milestones that we have before us and then there are a couple that we're working on now that we haven't announced yet.
Tuesday, December 7, 2010
Vitamin C For Macular Degeneration
by Admin
Some of the vitamins that can help when it comes to protecting eyesight and reducing or preventing age macular degeneration includes Vitamin C, E, Thiamine, Riboflavin, B-6, B12, Folic Acid, Niacin, Zinc, L-Taurine, Manganese, Copper, Selenium, Calcium, L-Glutathione, Rutin, Lycopene and Lutein. All of these vitamins have properties that help to increase eye health and increase the body’s ability to reduce the effects of macular degeneration for example these vitamins may help in the reduction of blood vessels or the reduction of Drusen that buildup between the macula and the retina. Improving your eyesight can also help to reduce symptoms in the beginning stages of macular degeneration.
Some of the vitamins that can help when it comes to protecting eyesight and reducing or preventing age macular degeneration includes Vitamin C, E, Thiamine, Riboflavin, B-6, B12, Folic Acid, Niacin, Zinc, L-Taurine, Manganese, Copper, Selenium, Calcium, L-Glutathione, Rutin, Lycopene and Lutein. All of these vitamins have properties that help to increase eye health and increase the body’s ability to reduce the effects of macular degeneration for example these vitamins may help in the reduction of blood vessels or the reduction of Drusen that buildup between the macula and the retina. Improving your eyesight can also help to reduce symptoms in the beginning stages of macular degeneration.
Sunday, November 28, 2010
Retinal Disease Treatments Double Over 10 Years
by:Jen Blackstock
When most people think of diabetes, the first thing to come to mind is rarely blindness, yet blindness is a very real complication of diabetes: Diabetes is actually the number one cause of new blindness in the United States.
Diabetic retinopathy happens when diabetes damages the tiny blood vessels inside the retina, which therefore stop feeding the retina properly, according to the American Foundation for the Blind. Symptoms can include blurry or double vision; rings, flashing lights or blank spots; dark or floating spots; pain or pressure in one or both of your eyes; and trouble seeing things out of the corners of your eyes. Forty percent of people with diabetes have some form of diabetic retinopathy.
With the rise in the number of people with diabetes and the aging American population, it is no surprise that the number of older Americans undergoing treatment for retinal conditions such as age-related macular degeneration (AMD) and diabetic retinopathy increased 192 percent between 1997 and 2007. Additionally, there has been a significant shift in the types of procedures being performed, a new study has found.
Age-related macular degeneration is a progressive disease of the retina that causes the loss of central vision. Both age-related macular degeneration and diabetic retinopathy can cause vision loss and blindness.
The study analyzed Medicare data from 1997 to 2007 and found that the number of retinal procedures increased 192 percent during that period. The largest year-to-year increase (20 percent) occurred between 2006 and 2007, according to the study published in the October issue of the journal Archives of Ophthalmology.
In terms of actual procedures performed, the largest increase was in treatments for neovascular, or "wet," AMD. New treatments for this condition include intravitreal therapy, or drug injections directly into the eye, of antibodies that block the formation of new blood vessels. From 1997 to 2001, only 5,000 of these procedures were performed each year. By 2007, the number had jumped to 812,413. Also increasing is the use of vitrectomy, a surgery to remove the gel inside the eye in order to treat retinal detachment -- increased 72 percent between 1997 and 2007.
"Retinal disease is highly prevalent among older individuals, and both age-related macular degeneration and diabetic retinopathy account for more than half the irreversible blindness in older Americans. The prevalence of both macular degeneration and diabetic retinopathy increases with age, and the number of Americans affected by these conditions is expected to increase substantially as the number of Americans older than 65 years doubles from 2010 to 2040," says study author Dr. Pradeep Ramulu, of Wilmer Eye Institute at Johns Hopkins University in Baltimore.
With the rise of cases of diabetes and the aging of the baby boomer population in the United States, eye care and blindness prevention is becoming increasingly important within the medical community.
When most people think of diabetes, the first thing to come to mind is rarely blindness, yet blindness is a very real complication of diabetes: Diabetes is actually the number one cause of new blindness in the United States.
Diabetic retinopathy happens when diabetes damages the tiny blood vessels inside the retina, which therefore stop feeding the retina properly, according to the American Foundation for the Blind. Symptoms can include blurry or double vision; rings, flashing lights or blank spots; dark or floating spots; pain or pressure in one or both of your eyes; and trouble seeing things out of the corners of your eyes. Forty percent of people with diabetes have some form of diabetic retinopathy.
With the rise in the number of people with diabetes and the aging American population, it is no surprise that the number of older Americans undergoing treatment for retinal conditions such as age-related macular degeneration (AMD) and diabetic retinopathy increased 192 percent between 1997 and 2007. Additionally, there has been a significant shift in the types of procedures being performed, a new study has found.
Age-related macular degeneration is a progressive disease of the retina that causes the loss of central vision. Both age-related macular degeneration and diabetic retinopathy can cause vision loss and blindness.
The study analyzed Medicare data from 1997 to 2007 and found that the number of retinal procedures increased 192 percent during that period. The largest year-to-year increase (20 percent) occurred between 2006 and 2007, according to the study published in the October issue of the journal Archives of Ophthalmology.
In terms of actual procedures performed, the largest increase was in treatments for neovascular, or "wet," AMD. New treatments for this condition include intravitreal therapy, or drug injections directly into the eye, of antibodies that block the formation of new blood vessels. From 1997 to 2001, only 5,000 of these procedures were performed each year. By 2007, the number had jumped to 812,413. Also increasing is the use of vitrectomy, a surgery to remove the gel inside the eye in order to treat retinal detachment -- increased 72 percent between 1997 and 2007.
"Retinal disease is highly prevalent among older individuals, and both age-related macular degeneration and diabetic retinopathy account for more than half the irreversible blindness in older Americans. The prevalence of both macular degeneration and diabetic retinopathy increases with age, and the number of Americans affected by these conditions is expected to increase substantially as the number of Americans older than 65 years doubles from 2010 to 2040," says study author Dr. Pradeep Ramulu, of Wilmer Eye Institute at Johns Hopkins University in Baltimore.
With the rise of cases of diabetes and the aging of the baby boomer population in the United States, eye care and blindness prevention is becoming increasingly important within the medical community.
Monday, November 22, 2010
New Techology Detects Retinal Disease
by Martha L. Hernández
McALLEN — For years, the only way for doctors into the back of the eye for a retina inspection involved special eye drops, which dilated the patient’s pupils and required the wearing of dark glasses for hours after the exam.
Now, scientists have developed the Optomap Retinal Exam, which eliminates the need for drop. Patients only see a quick, green flash of light.
“This test is a non-invasive way of doing it. We don’t put drops in your eyes, we just take a picture of the back of your eye and under 25 seconds (later), it gives us a 3D image. We can review the image with you on the computer (immediately after),” said Dr. Fiona Kolia, a therapeutic optometrist at Astoria Vision Source.
“We can look at it with different filters. This test is very important because it allows us to tell you about the health not only of your eye — where we can detect (diseases like) glaucoma (or) macular degeneration, any holes or tears, anything that is in the eye that shouldn’t be there — it also tells us about the health of your body,” Kolia said.
The new technology has detected other medical conditions in people seeking glasses or contacts.
“For example, a young person, healthy, walked in and he had a hemorrhage in his eye that is caused by high blood pressure, and high blood pressure is a silent killer, you refer them (to their family doctor) and they can start to get treated and take care of themselves,” Kolia said. Undetected high blood pressure can lead to strokes and other serious complications, Kolia noted.
“Sometimes we are the first to detect if the people have signs of high blood pressure, diabetes, high cholesterol, any arteriosclerosis in the eye and we refer them to their family physician” Kolia said.
Kolia is the only optometrist south of Corpus Christi that has an Optomap.
“Sometimes people just don’t see well and they might think it’s just their glasses” Kolia said. “There was a gentleman that had a macular degeneration that needed to be treated … but sometime in younger people (that) kind of problem happens due to high stress and the macular area (center of the eye) can become swollen and you can lose your central vision (if you do not treat it),” Kolia said.
“What we hope to do is be able to screen a lot of people, I think that in this area it is very important for diabetics. We want to it as a tool and make people aware that an eye exam not only involves getting you a better pair of glasses, it involves looking at the interior structures of the eye and behind the eye,” which can aid in the detection of numerous health issues, Kolia said.
Insurance companies do not typically cover treatment with an Optomap. If there is a definite medical diagnosis it may be billed as a retinal photo in some instances with some insurance plans. Patients without insurance pay $37 for the test.
“In a lot of people who are nearsighted, the eyeball elongates, so it is important to look behind the eye because they can develop a retinal detachment,” Kolia said.
Kolia said the Optomap likely would be added to the regular battery of tests conducted by optometrists and ophthalmologists during routine eye exams as the technology comes into more widespread use.
McALLEN — For years, the only way for doctors into the back of the eye for a retina inspection involved special eye drops, which dilated the patient’s pupils and required the wearing of dark glasses for hours after the exam.
Now, scientists have developed the Optomap Retinal Exam, which eliminates the need for drop. Patients only see a quick, green flash of light.
“This test is a non-invasive way of doing it. We don’t put drops in your eyes, we just take a picture of the back of your eye and under 25 seconds (later), it gives us a 3D image. We can review the image with you on the computer (immediately after),” said Dr. Fiona Kolia, a therapeutic optometrist at Astoria Vision Source.
“We can look at it with different filters. This test is very important because it allows us to tell you about the health not only of your eye — where we can detect (diseases like) glaucoma (or) macular degeneration, any holes or tears, anything that is in the eye that shouldn’t be there — it also tells us about the health of your body,” Kolia said.
The new technology has detected other medical conditions in people seeking glasses or contacts.
“For example, a young person, healthy, walked in and he had a hemorrhage in his eye that is caused by high blood pressure, and high blood pressure is a silent killer, you refer them (to their family doctor) and they can start to get treated and take care of themselves,” Kolia said. Undetected high blood pressure can lead to strokes and other serious complications, Kolia noted.
“Sometimes we are the first to detect if the people have signs of high blood pressure, diabetes, high cholesterol, any arteriosclerosis in the eye and we refer them to their family physician” Kolia said.
Kolia is the only optometrist south of Corpus Christi that has an Optomap.
“Sometimes people just don’t see well and they might think it’s just their glasses” Kolia said. “There was a gentleman that had a macular degeneration that needed to be treated … but sometime in younger people (that) kind of problem happens due to high stress and the macular area (center of the eye) can become swollen and you can lose your central vision (if you do not treat it),” Kolia said.
“What we hope to do is be able to screen a lot of people, I think that in this area it is very important for diabetics. We want to it as a tool and make people aware that an eye exam not only involves getting you a better pair of glasses, it involves looking at the interior structures of the eye and behind the eye,” which can aid in the detection of numerous health issues, Kolia said.
Insurance companies do not typically cover treatment with an Optomap. If there is a definite medical diagnosis it may be billed as a retinal photo in some instances with some insurance plans. Patients without insurance pay $37 for the test.
“In a lot of people who are nearsighted, the eyeball elongates, so it is important to look behind the eye because they can develop a retinal detachment,” Kolia said.
Kolia said the Optomap likely would be added to the regular battery of tests conducted by optometrists and ophthalmologists during routine eye exams as the technology comes into more widespread use.
Monday, November 15, 2010
Limited Retinal Translocation for Wet Macular Degeneration
Posted by Administration
Limited Retinal Translocation-Limited retinal translocation is another treatment aimed at wet macular degeneration. In this procedure the retina is actually moved somewhat to allow laser treatments to be applied more successfully to abnormal blood vessel growth. The procedure is still in the macular degeneration treatments developmental stages in terms of approval for commercial applications. Surgical options for dry macular degeneration are proposed periodically. The methodologies change from procedure to procedure, but the general idea is the same.
Limited Retinal Translocation-Limited retinal translocation is another treatment aimed at wet macular degeneration. In this procedure the retina is actually moved somewhat to allow laser treatments to be applied more successfully to abnormal blood vessel growth. The procedure is still in the macular degeneration treatments developmental stages in terms of approval for commercial applications. Surgical options for dry macular degeneration are proposed periodically. The methodologies change from procedure to procedure, but the general idea is the same.
Thursday, November 4, 2010
Eye Implant breakthrough
By Andrew Hough
Eye implant breakthrough: scientific advances towards a blindness cures
An eye test is the only way to diagnose glaucoma, the leading cause of blindness in Britain.
* Stem cells grown on contact lenses could be a cure for a common cause of blindness, claim scientists. Australian researchers said that the world breakthrough could "dramatically improve" the sight of patients with damage to their cornea – the clear outer shell of the eye – caused by disease or injury.
The research team removed tissue with regenerative stem cells from patients' own eyes and then multiplied them in the laboratory on the surface of a contact lens. This was then placed back onto the damaged cornea for 10 days, during which the cells, which can turn into any other sort of cell, were able to recolonise and "patch" the damaged eye surface. Within weeks the patients saw dramatic improvements in their vision. If early findings bear out then the treatment could be affective for thousands of patients in Britain and is so cheap it could be used for millions more in the Third World.
* Artificial corneas grown in the laboratory were transplanted into patient's eyes for the first time in an operation, scientists reported. The new technique involved growing human tissue or collagen in the laboratory and then shaping it using a contact lens mould.
Damaged and scarred tissue from the front of the eye is then removed and the "biosynthetic" replacement is stitched in its place. Eventually existing cells and nerves in the eye grow over the artificial cornea incorporating it fully into the eye.
* Eye cells that are sensitive to light were produced from skin in a breakthrough that could eventually lead to treatments for blindness, scientists reported in August. Researchers genetically “reprogrammed” human skin cells to possess the same properties as those that make up the retina.
The process involved first turning them into pluripotent stem (IPS) cells, which have the potential to develop into virtually every kind of tissue in the body. By exposing the IPS cells to a specific cocktail of chemicals, the scientists then caused them to grow into partially developed retina cells – the light-sensitive cells at the back of the eye which transmit nerve signals to the brain.
* Patients who were left blinded after chemical accidents have had their sight restored using corneas grown from their own stem cells, scientists claimed in June. In the largest study of its kind, Italian researchers said they restored the sight of patients left blinded or suffered severely impaired vision, after suffering chemical burns.
Experts said the study, undertaken between 1998 and 2007, offers new hope to the thousands of people who suffer chemical burns on their corneas from heavy-duty cleansers or other substances at work or at home. The research is also being hailed as a key breakthrough in scientific regeneration that could give hope to other patients with otherwise irreversible eyesight.
* Also in June, a new study suggested a simple way to stop you eyesight deterioriating - drinking red wine. Researchers have found that a substance found in grapes and other fruits could protect blood vessels in the eye being damaged by old age. It is effective because the compound, known as resveratrol, stops the blood vessels from being damaged.
The substance, which has been linked to anti-ageing and cancer protection in the past, is believed to work because it protects against abnormal angiogenesis – the formation of damaged or mutated blood vessels. This condition is linked to cancer, heart disease and eye diseases such as age-related macular degeneration. In the study, reported in the New England Journal of Medicine, researchers successfully extracted adult stem cells from healthy eye tissue before growing additional stem cells that were placed over damaged eye tissue.
* Gene therapy was used by American scientists to improve the vision of children with hereditary blindness. US doctors treating 12 patients with a rare genetic eye disorder were able to significantly improve vision in the youngest, according to medical journal The Lancet. The research, which builds on work carried out by doctors at London's Moorfields Eye Hospital, focused on Leber's congenital amaurosis (LCA), a disorder which causes gradual deterioration in vision and can lead to blindness by the time the patient is 20. It occurs when faulty genes, called RPE65, stop the layer of cells at the back of the eye working and affects approximately one in 80,000 people. It is responsible for one in 10 severe sight disorders in children.
* Scientists cured colour blindness in monkeys, in what some were signalling has new hope for millions of sufferers of the condition. Researchers reported last September that they cured the animals using a treatment called gene therapy. A harmless virus which delivers corrective genes to the retina was injected into the eyes of two squirrel monkeys, Dalton and Sam, who had been colour blind since birth. Within weeks a protein produced by the corrective genes allowed both monkeys to make out reds and greens for the first time. They can still see the colours two years later. The breakthrough could also have implications for other damaging genetic eye defects, including those which can cause blindness, after researchers proved for the first time that the brain can “rewire” itself to see things it has never been able to before.
* A new eye drop treatment was offered to help preserve the sight of thousands of people at risk of going blind due to glaucoma, scientists reported. The drops were first of their kind that avoid unpleasant side effects which deter up to a third of patients from continuing their treatment.
Many patients simply refuse to apply the drops because of the discomfort, thereby putting themselves at risk of vision loss. Regular use of the eye drops can keep the condition under control for a patient's life time. Without them, a patient can go blind in five to 10 years. When the disease becomes too advanced the only remedy is surgery, which is risky and may itself result in blindness.
Eye implant breakthrough: scientific advances towards a blindness cures
An eye test is the only way to diagnose glaucoma, the leading cause of blindness in Britain.
* Stem cells grown on contact lenses could be a cure for a common cause of blindness, claim scientists. Australian researchers said that the world breakthrough could "dramatically improve" the sight of patients with damage to their cornea – the clear outer shell of the eye – caused by disease or injury.
The research team removed tissue with regenerative stem cells from patients' own eyes and then multiplied them in the laboratory on the surface of a contact lens. This was then placed back onto the damaged cornea for 10 days, during which the cells, which can turn into any other sort of cell, were able to recolonise and "patch" the damaged eye surface. Within weeks the patients saw dramatic improvements in their vision. If early findings bear out then the treatment could be affective for thousands of patients in Britain and is so cheap it could be used for millions more in the Third World.
* Artificial corneas grown in the laboratory were transplanted into patient's eyes for the first time in an operation, scientists reported. The new technique involved growing human tissue or collagen in the laboratory and then shaping it using a contact lens mould.
Damaged and scarred tissue from the front of the eye is then removed and the "biosynthetic" replacement is stitched in its place. Eventually existing cells and nerves in the eye grow over the artificial cornea incorporating it fully into the eye.
* Eye cells that are sensitive to light were produced from skin in a breakthrough that could eventually lead to treatments for blindness, scientists reported in August. Researchers genetically “reprogrammed” human skin cells to possess the same properties as those that make up the retina.
The process involved first turning them into pluripotent stem (IPS) cells, which have the potential to develop into virtually every kind of tissue in the body. By exposing the IPS cells to a specific cocktail of chemicals, the scientists then caused them to grow into partially developed retina cells – the light-sensitive cells at the back of the eye which transmit nerve signals to the brain.
* Patients who were left blinded after chemical accidents have had their sight restored using corneas grown from their own stem cells, scientists claimed in June. In the largest study of its kind, Italian researchers said they restored the sight of patients left blinded or suffered severely impaired vision, after suffering chemical burns.
Experts said the study, undertaken between 1998 and 2007, offers new hope to the thousands of people who suffer chemical burns on their corneas from heavy-duty cleansers or other substances at work or at home. The research is also being hailed as a key breakthrough in scientific regeneration that could give hope to other patients with otherwise irreversible eyesight.
* Also in June, a new study suggested a simple way to stop you eyesight deterioriating - drinking red wine. Researchers have found that a substance found in grapes and other fruits could protect blood vessels in the eye being damaged by old age. It is effective because the compound, known as resveratrol, stops the blood vessels from being damaged.
The substance, which has been linked to anti-ageing and cancer protection in the past, is believed to work because it protects against abnormal angiogenesis – the formation of damaged or mutated blood vessels. This condition is linked to cancer, heart disease and eye diseases such as age-related macular degeneration. In the study, reported in the New England Journal of Medicine, researchers successfully extracted adult stem cells from healthy eye tissue before growing additional stem cells that were placed over damaged eye tissue.
* Gene therapy was used by American scientists to improve the vision of children with hereditary blindness. US doctors treating 12 patients with a rare genetic eye disorder were able to significantly improve vision in the youngest, according to medical journal The Lancet. The research, which builds on work carried out by doctors at London's Moorfields Eye Hospital, focused on Leber's congenital amaurosis (LCA), a disorder which causes gradual deterioration in vision and can lead to blindness by the time the patient is 20. It occurs when faulty genes, called RPE65, stop the layer of cells at the back of the eye working and affects approximately one in 80,000 people. It is responsible for one in 10 severe sight disorders in children.
* Scientists cured colour blindness in monkeys, in what some were signalling has new hope for millions of sufferers of the condition. Researchers reported last September that they cured the animals using a treatment called gene therapy. A harmless virus which delivers corrective genes to the retina was injected into the eyes of two squirrel monkeys, Dalton and Sam, who had been colour blind since birth. Within weeks a protein produced by the corrective genes allowed both monkeys to make out reds and greens for the first time. They can still see the colours two years later. The breakthrough could also have implications for other damaging genetic eye defects, including those which can cause blindness, after researchers proved for the first time that the brain can “rewire” itself to see things it has never been able to before.
* A new eye drop treatment was offered to help preserve the sight of thousands of people at risk of going blind due to glaucoma, scientists reported. The drops were first of their kind that avoid unpleasant side effects which deter up to a third of patients from continuing their treatment.
Many patients simply refuse to apply the drops because of the discomfort, thereby putting themselves at risk of vision loss. Regular use of the eye drops can keep the condition under control for a patient's life time. Without them, a patient can go blind in five to 10 years. When the disease becomes too advanced the only remedy is surgery, which is risky and may itself result in blindness.
Saturday, October 30, 2010
Telescope Implant Improves Vision in Macular Degeneration
by Kathleen Louden
(Chicago, Illinois) — People with end-stage age-related macular degeneration (AMD) have improved visual acuity and quality of life after receiving an intraocular implant containing a tiny telescope in 1 eye, new research shows. An ophthalmologist who participated in the clinical trials presented the unpublished results here at the American Academy of Ophthalmology and Middle East Africa Council of Ophthalmology 2010 Joint Meeting.
The telescope implant improves vision in "a disease in which the patient is legally blind and has no surgical or medical alternatives," the presenter, Stephen Lane, MD, told Medscape Medical News. He was a medical monitor for the pivotal trials and is an adjunct professor of ophthalmology at the University of Minnesota, Minneapolis.
In July, the US Food and Drug Administration approved the telescope implant, also called the implantable miniature telescope (VisionCare Ophthalmic Technologies), to improve vision in some patients with end-stage AMD.
Telescope Magnifies Images More Than 2 Times
"The reason why this [device] works is a magnification effect, so the central scotoma can be overcome," Dr. Lane told meeting attendees.
This pea-sized implant, which replaces the natural lens, magnifies images greater than 2 times and projects the images onto a healthy part of the retina, according to the device manufacturer. It is available in 2 models: 1 that provides 2.2 times the magnification and another that gives 2.7 times magnification. Patients use the eye that received the implant for central vision and use the untreated fellow eye for peripheral vision.
To be eligible for this class 3 medical device, patients must have bilateral geographic atrophy or "post-wet" AMD disciform scars and must not yet have had cataract surgery, although they can have cataract, Dr. Lane said. Other eligibility criteria, according to the US Food and Drug Administration, include age 75 years or older and "stable severe to profound vision impairment" resulting from bilateral central scotoma.
In a multicenter clinical trial of more than 200 patients who received the implant, the mean best corrected visual acuity before implantation was worse than 20/300, Dr. Lane said. More than 80% of patients had at least a 2-line improvement in visual acuity on the Snellen chart 1 year after surgery, and 46% of patients improved 4 lines or more at 1 year, he reported. Most of those patients, according to Dr. Lane, maintained their improved visual acuity 2 years postoperatively (75% with 2 lines or better and 43% with 4 or more lines of improvement).
"Quality of life gains also are clinically meaningful," Dr. Lane said. "Patients were less dependent, better able to recognize people, and better able to...do activities of daily living."
Endothelial Cell Loss Possible
A possible complication of the implant is the loss of corneal endothelial cells. In the study, there was a 20% loss of epithelial cells, which Dr. Lane called "a little high." He said ophthalmologists should inform their patients that substantial endothelial cell loss can lead to corneal decompensation and the need for a corneal transplant.
A Michigan ophthalmologist who did not participate in the studies, George Williams, MD, said in an interview that study investigators told him that most patients in the studies tolerated the implant well and found it very helpful.
However, the device is for "a select group of patients with end-stage AMD," said Dr. Williams, chairman of the Department of Ophthalmology at Oakland University William Beaumont School of Medicine, Royal Oak, Michigan.
He mentioned, as did Dr. Lane, that patients need to undergo an evaluation to determine whether they can benefit from this device, which involves a trial with an external telescope.
"Only 1 in 5 patients who are screened actually end up getting the device," Dr. Williams told Medscape Medical News.
After the surgery, patients must receive training with a low-vision specialist. "It's hard to walk around with a telescope in your eye," Dr. Williams said.
Patients who did not tolerate the implant were those who could not adjust to using 1 eye for near-vision tasks and the other eye for distance vision, Dr. Lane said during the meeting.
(Chicago, Illinois) — People with end-stage age-related macular degeneration (AMD) have improved visual acuity and quality of life after receiving an intraocular implant containing a tiny telescope in 1 eye, new research shows. An ophthalmologist who participated in the clinical trials presented the unpublished results here at the American Academy of Ophthalmology and Middle East Africa Council of Ophthalmology 2010 Joint Meeting.
The telescope implant improves vision in "a disease in which the patient is legally blind and has no surgical or medical alternatives," the presenter, Stephen Lane, MD, told Medscape Medical News. He was a medical monitor for the pivotal trials and is an adjunct professor of ophthalmology at the University of Minnesota, Minneapolis.
In July, the US Food and Drug Administration approved the telescope implant, also called the implantable miniature telescope (VisionCare Ophthalmic Technologies), to improve vision in some patients with end-stage AMD.
Telescope Magnifies Images More Than 2 Times
"The reason why this [device] works is a magnification effect, so the central scotoma can be overcome," Dr. Lane told meeting attendees.
This pea-sized implant, which replaces the natural lens, magnifies images greater than 2 times and projects the images onto a healthy part of the retina, according to the device manufacturer. It is available in 2 models: 1 that provides 2.2 times the magnification and another that gives 2.7 times magnification. Patients use the eye that received the implant for central vision and use the untreated fellow eye for peripheral vision.
To be eligible for this class 3 medical device, patients must have bilateral geographic atrophy or "post-wet" AMD disciform scars and must not yet have had cataract surgery, although they can have cataract, Dr. Lane said. Other eligibility criteria, according to the US Food and Drug Administration, include age 75 years or older and "stable severe to profound vision impairment" resulting from bilateral central scotoma.
In a multicenter clinical trial of more than 200 patients who received the implant, the mean best corrected visual acuity before implantation was worse than 20/300, Dr. Lane said. More than 80% of patients had at least a 2-line improvement in visual acuity on the Snellen chart 1 year after surgery, and 46% of patients improved 4 lines or more at 1 year, he reported. Most of those patients, according to Dr. Lane, maintained their improved visual acuity 2 years postoperatively (75% with 2 lines or better and 43% with 4 or more lines of improvement).
"Quality of life gains also are clinically meaningful," Dr. Lane said. "Patients were less dependent, better able to recognize people, and better able to...do activities of daily living."
Endothelial Cell Loss Possible
A possible complication of the implant is the loss of corneal endothelial cells. In the study, there was a 20% loss of epithelial cells, which Dr. Lane called "a little high." He said ophthalmologists should inform their patients that substantial endothelial cell loss can lead to corneal decompensation and the need for a corneal transplant.
A Michigan ophthalmologist who did not participate in the studies, George Williams, MD, said in an interview that study investigators told him that most patients in the studies tolerated the implant well and found it very helpful.
However, the device is for "a select group of patients with end-stage AMD," said Dr. Williams, chairman of the Department of Ophthalmology at Oakland University William Beaumont School of Medicine, Royal Oak, Michigan.
He mentioned, as did Dr. Lane, that patients need to undergo an evaluation to determine whether they can benefit from this device, which involves a trial with an external telescope.
"Only 1 in 5 patients who are screened actually end up getting the device," Dr. Williams told Medscape Medical News.
After the surgery, patients must receive training with a low-vision specialist. "It's hard to walk around with a telescope in your eye," Dr. Williams said.
Patients who did not tolerate the implant were those who could not adjust to using 1 eye for near-vision tasks and the other eye for distance vision, Dr. Lane said during the meeting.
Tuesday, October 26, 2010
Gene Therapy/ Treatment for Visual Impairment
Gene Therapy For Visual Impairment
By: Mark Burnsy
In modern society where most people are educated, eyesight problems inevitably proliferate, due to the fact that they have spent more time in reading. TV and computers are also incentives of the skyrocketed eyesight problems. Owing to the invention of eyeglasses and contact lenses, people with nearsightedness, farsightedness, astigmatism and presbyopia are able to view a clear world as well. Additionally, fast developed, eyeglass manufactures achieve advancement in glare reduction and unwanted wavelengths of light elimination.
However, eyeglasses and contacts can not serve as helps for vision improvement of people suffering from eye diseases, such as Macular Degeneration and Diabetic Retinopathy. Recently, a medical treatment is developed, which is also able to treat visual impairments. Avastin is a drug that was originally used in Colo-rectal cancer treatments but is found to have an ability to improve the vision in patients with Macular Degeneration, Diabetic Retinopathy and other vascular related retinal diseases. What's more, many other new drugs are brought about in succession as well, for example, the non steroidal anti inflammatory drugs can reduce retinal inflammation and cyst formations.
There are some people whose eye diseases arise from within the patients, genetic and congenital disorders. They pose a great challenge to eye doctors and surgeons. Luckily, gene therapy is found to be able to dramatically improve those patients' vision. The procedure is performed at the Scheie Eye Institute in Philadelphia and the patients formerly suffering from Leber's Congenital Amaurosis claim that he could read letters on an eye chart already after such a procedure. Then the news was published in the New England Journal of Medicine, on which the cause of Leber's Congenital Amaurosis and how the surgery achieves an success are recorded. It is stated that a lack of RPE 65 gene prevents protein production which is required for the retinal tissue to absorb and process the light into vision. A normal RPE is injected in the gene therapy to restore the protein production. After two weeks, the patients can mostly view more clearly than they did before. Possible complications of gene therapy include sensitivity to light.
In spit that it is just a successful case of Leber's Congenital Amaurosis treatment, it gives hopes to other eye diseases originated from gene disorders. Researches concerned are under procession. The application of gene therapy in visual impairment will be a great success in the near future.
By: Mark Burnsy
In modern society where most people are educated, eyesight problems inevitably proliferate, due to the fact that they have spent more time in reading. TV and computers are also incentives of the skyrocketed eyesight problems. Owing to the invention of eyeglasses and contact lenses, people with nearsightedness, farsightedness, astigmatism and presbyopia are able to view a clear world as well. Additionally, fast developed, eyeglass manufactures achieve advancement in glare reduction and unwanted wavelengths of light elimination.
However, eyeglasses and contacts can not serve as helps for vision improvement of people suffering from eye diseases, such as Macular Degeneration and Diabetic Retinopathy. Recently, a medical treatment is developed, which is also able to treat visual impairments. Avastin is a drug that was originally used in Colo-rectal cancer treatments but is found to have an ability to improve the vision in patients with Macular Degeneration, Diabetic Retinopathy and other vascular related retinal diseases. What's more, many other new drugs are brought about in succession as well, for example, the non steroidal anti inflammatory drugs can reduce retinal inflammation and cyst formations.
There are some people whose eye diseases arise from within the patients, genetic and congenital disorders. They pose a great challenge to eye doctors and surgeons. Luckily, gene therapy is found to be able to dramatically improve those patients' vision. The procedure is performed at the Scheie Eye Institute in Philadelphia and the patients formerly suffering from Leber's Congenital Amaurosis claim that he could read letters on an eye chart already after such a procedure. Then the news was published in the New England Journal of Medicine, on which the cause of Leber's Congenital Amaurosis and how the surgery achieves an success are recorded. It is stated that a lack of RPE 65 gene prevents protein production which is required for the retinal tissue to absorb and process the light into vision. A normal RPE is injected in the gene therapy to restore the protein production. After two weeks, the patients can mostly view more clearly than they did before. Possible complications of gene therapy include sensitivity to light.
In spit that it is just a successful case of Leber's Congenital Amaurosis treatment, it gives hopes to other eye diseases originated from gene disorders. Researches concerned are under procession. The application of gene therapy in visual impairment will be a great success in the near future.
Sunday, October 10, 2010
Zeaxanthin For Macular Degeneration Prevention and Treatment for Dry AMD
by Forrestal
Most ophthalmologists recommend the antioxidants lutein and zeaxanthin for macular degeneration that is age related, commonly referred to as AMD. It is unusual for doctor’s to recommend nutritional supplements of any kind, unless a person has an outright deficiency, but AMD is a unique condition.
There are no effective treatments for one type of AMD (dry), but there are some partially effective treatments for wet AMD. Together, these two are the major causes of blindness in the elderly. The wet form is the most severe, if not treated early.
In wet AMD, blood vessels grow up and behind the retina, an area responsible for gathering light and transmitting signals to the brain, resulting in sight. The blood vessels often rupture and leak blood and protein below the macula, a very sensitive area within the retina.
Eventually, bleeding, leaking and scarring causes irreversible damage to the light receptors (rods and cones). Rapid vision loss is experienced if it is left untreated. Laser treatment and drugs that inhibit blood vessel growth are usually recommended.
Generally, doctors recommend lutein and zeaxanthin for macular degeneration that is of the dry type. Dry AMD is much more common than wet. It is caused by a build up of yellow deposits called drusen on the retina.
In nature lutein and zeaxanthin are pigments or colors. They are normally present in the retina, with zeaxanthin being concentrated in the macula and lutein more highly concentrated in the periphery of the retina. There roles within the eye are not well understood, but they seem to help reduce or prevent the build up of drusen.
Drusen is similar in composition to the deposits that are found in the brains of Alzheimer’s patients and the plaque that is present in atherosclerosis. People with either of those two conditions have a higher risk of developing dry AMD.
Some doctors recommend taking lutein and zeaxanthin for macular degeneration prevention, particularly to their patients that have a family history of the disease. But, since the drusen are similar to the deposits that cause Alzheimer’s and heart disease, other antioxidants may be beneficial, as well.
Curcumin, an antioxidant present in the spice turmeric, is currently being studied for its benefit in Alzheimer’s disease. Not only does it prevent the accumulation of the plaque, it breaks it up. It might be able to break up the drusen in AMD, too.
One study indicates that the ideal combination of nutrients is omega 3 fatty acids, beta carotene, vitamin E, lutein and zeaxanthin for macular degeneration. Omega 3 fatty acids, particularly DHA, are the most abundant fatty acids present in the retina. Beta-carotene is converted by the body to vitamin A, which is essential for good vision. Vitamin E is well-known for its antioxidant activity.
Prevention is worth a pound of cure, they say. In order to prevent AMD, people should lower their total fat intake, and increase their nutrient intake. This may help reduce the risk of many other diseases, as well. Taking zeaxanthin for macular degeneration prevention is a good idea. Taking a multi-nutritional supplement that contains it, is a great one.
Most ophthalmologists recommend the antioxidants lutein and zeaxanthin for macular degeneration that is age related, commonly referred to as AMD. It is unusual for doctor’s to recommend nutritional supplements of any kind, unless a person has an outright deficiency, but AMD is a unique condition.
There are no effective treatments for one type of AMD (dry), but there are some partially effective treatments for wet AMD. Together, these two are the major causes of blindness in the elderly. The wet form is the most severe, if not treated early.
In wet AMD, blood vessels grow up and behind the retina, an area responsible for gathering light and transmitting signals to the brain, resulting in sight. The blood vessels often rupture and leak blood and protein below the macula, a very sensitive area within the retina.
Eventually, bleeding, leaking and scarring causes irreversible damage to the light receptors (rods and cones). Rapid vision loss is experienced if it is left untreated. Laser treatment and drugs that inhibit blood vessel growth are usually recommended.
Generally, doctors recommend lutein and zeaxanthin for macular degeneration that is of the dry type. Dry AMD is much more common than wet. It is caused by a build up of yellow deposits called drusen on the retina.
In nature lutein and zeaxanthin are pigments or colors. They are normally present in the retina, with zeaxanthin being concentrated in the macula and lutein more highly concentrated in the periphery of the retina. There roles within the eye are not well understood, but they seem to help reduce or prevent the build up of drusen.
Drusen is similar in composition to the deposits that are found in the brains of Alzheimer’s patients and the plaque that is present in atherosclerosis. People with either of those two conditions have a higher risk of developing dry AMD.
Some doctors recommend taking lutein and zeaxanthin for macular degeneration prevention, particularly to their patients that have a family history of the disease. But, since the drusen are similar to the deposits that cause Alzheimer’s and heart disease, other antioxidants may be beneficial, as well.
Curcumin, an antioxidant present in the spice turmeric, is currently being studied for its benefit in Alzheimer’s disease. Not only does it prevent the accumulation of the plaque, it breaks it up. It might be able to break up the drusen in AMD, too.
One study indicates that the ideal combination of nutrients is omega 3 fatty acids, beta carotene, vitamin E, lutein and zeaxanthin for macular degeneration. Omega 3 fatty acids, particularly DHA, are the most abundant fatty acids present in the retina. Beta-carotene is converted by the body to vitamin A, which is essential for good vision. Vitamin E is well-known for its antioxidant activity.
Prevention is worth a pound of cure, they say. In order to prevent AMD, people should lower their total fat intake, and increase their nutrient intake. This may help reduce the risk of many other diseases, as well. Taking zeaxanthin for macular degeneration prevention is a good idea. Taking a multi-nutritional supplement that contains it, is a great one.
Friday, July 16, 2010
Gene Therapy for Eye Diseases
The pharmaceutical giant Genzyme has started a clinical trial to see whether a drug to treat macular generation could be delivered via long-lasting gene therapy rather than monthly injections.
Eye colors: Drusen, the yellow flecks in this image of the retina, are common in people with age-related macular degeneration. These flecks are made up of proteins involved in the part of the immune system called the complement system, which has also been implicated in the disease by genetic studies.
A drug called Lucentis, made by Genetech, has proved effective at treating the wet form of age-related macular degeneration, which can lead to blindness. Some 200,000 Americans a year are diagnosed with the disease. But Lucentis has to be injected into the eye every month or two, a burden for patients and doctors.
Lucentis binds to and neutralizes a wound-healing growth factor known as VEGF. This binding action stalls the excess growth of blood vessels in the eye that characterizes age-related macular degeneration. Genzyme's gene therapy drug, officially called AAV2-sFLT01, would insinuate itself into the patient's retinal cell to produce the same VEGF-binding protein as Lucentis over far longer periods--up to several years.
A phase 1 clinical trial of Genzyme's gene therapy treatment began at the end of May. Three patients received the treatment, according to Sam Wadsworth, a Genzyme group vice president in charge of gene and cell therapy. Preliminary results should be available in about a year.
The trial is one of a handful worldwide seeking to prove the effectiveness of gene therapy for eye diseases. The Genzyme trial also involves using new type of virus as the delivery mechanism. Early results of a federally funded trial to deliver normal-functioning genes to patients with a rare retinal disease known as type 2 leber congenital amaurosis, or LCA, have confirmed that this "viral vector" has merit for eye treatments, several researchers say.
The LCA trials "demonstrated success both in terms of safety and ability to introduce the gene and have efficacy and success," said Jeffrey S. Heier, an assistant professor at Tufts University School of Medicine and director of retinal research at Ophthalmic Consultants of Boston, a private practice group, who is involved in the Genzyme research. "This study is taking the virus vector that they used, and [Genzyme has] taken what has really been the success of the anti-VEGF story and they've packaged the two together."
Eyes have been an early target for gene therapy because they are small--meaning they require relatively little active dose, they are self-contained, and because the tools of eye surgery have advanced enough to make the treatments possible. The drug has to be delivered to the retina, a thin film lining the inner wall of the eye. Instrumentation has improved in recent years to allow injections through the retina without piercing it, said Shalesh Kaushal, chairman of ophthalmology at University of Massachusetts Memorial Medical Center and UMass Medical School.
To Kaushal, who is involved in the Genzyme study as well as the LCA research, the big challenge will be broadening the use of gene therapy to dozens more diseases, and using that understanding to eventually reach beyond the eye. "If one could understand those fundamental cellular, biochemical events and identify targets, you might have the chance to treat many diseases with a single gene-therapy construct," Kaushal said.
Earlier gene therapy programs used a type of virus called adenovirus to target genes, but both the LCA and Genzyme trials are using adeno-associated virus, which is far less inflammatory and which expresses itself over longer periods than adenovirus, therefore making the treatment last longer, Wadsworth said. Viruses are used to deliver gene therapies because they are adept at getting through cell walls.
VEGF is involved in vascular cell growth throughout the body, and its expression increases in the presence of a wound. Studies have shown that with Lucentis, virtually all the VEGF-binding protein stays within the eye, and does not significantly affect VEGF levels elsewhere in the body, Wadsworth says. Genzyme's drug will provide even lower levels of the VEGF-binding protein, so it's expected that the drug will not have any adverse affects throughout the body, he said.
The trick will be getting the cells to produce enough VEGF-binding protein to help patients, said Peter Campochiaro, a professor at the Wilmer Eye Institute at Johns Hopkins Medicine, who is involved in the research. In addition to establishing safety, the current phase 1 trial will explore four different doses of the study
Eye colors: Drusen, the yellow flecks in this image of the retina, are common in people with age-related macular degeneration. These flecks are made up of proteins involved in the part of the immune system called the complement system, which has also been implicated in the disease by genetic studies.
A drug called Lucentis, made by Genetech, has proved effective at treating the wet form of age-related macular degeneration, which can lead to blindness. Some 200,000 Americans a year are diagnosed with the disease. But Lucentis has to be injected into the eye every month or two, a burden for patients and doctors.
Lucentis binds to and neutralizes a wound-healing growth factor known as VEGF. This binding action stalls the excess growth of blood vessels in the eye that characterizes age-related macular degeneration. Genzyme's gene therapy drug, officially called AAV2-sFLT01, would insinuate itself into the patient's retinal cell to produce the same VEGF-binding protein as Lucentis over far longer periods--up to several years.
A phase 1 clinical trial of Genzyme's gene therapy treatment began at the end of May. Three patients received the treatment, according to Sam Wadsworth, a Genzyme group vice president in charge of gene and cell therapy. Preliminary results should be available in about a year.
The trial is one of a handful worldwide seeking to prove the effectiveness of gene therapy for eye diseases. The Genzyme trial also involves using new type of virus as the delivery mechanism. Early results of a federally funded trial to deliver normal-functioning genes to patients with a rare retinal disease known as type 2 leber congenital amaurosis, or LCA, have confirmed that this "viral vector" has merit for eye treatments, several researchers say.
The LCA trials "demonstrated success both in terms of safety and ability to introduce the gene and have efficacy and success," said Jeffrey S. Heier, an assistant professor at Tufts University School of Medicine and director of retinal research at Ophthalmic Consultants of Boston, a private practice group, who is involved in the Genzyme research. "This study is taking the virus vector that they used, and [Genzyme has] taken what has really been the success of the anti-VEGF story and they've packaged the two together."
Eyes have been an early target for gene therapy because they are small--meaning they require relatively little active dose, they are self-contained, and because the tools of eye surgery have advanced enough to make the treatments possible. The drug has to be delivered to the retina, a thin film lining the inner wall of the eye. Instrumentation has improved in recent years to allow injections through the retina without piercing it, said Shalesh Kaushal, chairman of ophthalmology at University of Massachusetts Memorial Medical Center and UMass Medical School.
To Kaushal, who is involved in the Genzyme study as well as the LCA research, the big challenge will be broadening the use of gene therapy to dozens more diseases, and using that understanding to eventually reach beyond the eye. "If one could understand those fundamental cellular, biochemical events and identify targets, you might have the chance to treat many diseases with a single gene-therapy construct," Kaushal said.
Earlier gene therapy programs used a type of virus called adenovirus to target genes, but both the LCA and Genzyme trials are using adeno-associated virus, which is far less inflammatory and which expresses itself over longer periods than adenovirus, therefore making the treatment last longer, Wadsworth said. Viruses are used to deliver gene therapies because they are adept at getting through cell walls.
VEGF is involved in vascular cell growth throughout the body, and its expression increases in the presence of a wound. Studies have shown that with Lucentis, virtually all the VEGF-binding protein stays within the eye, and does not significantly affect VEGF levels elsewhere in the body, Wadsworth says. Genzyme's drug will provide even lower levels of the VEGF-binding protein, so it's expected that the drug will not have any adverse affects throughout the body, he said.
The trick will be getting the cells to produce enough VEGF-binding protein to help patients, said Peter Campochiaro, a professor at the Wilmer Eye Institute at Johns Hopkins Medicine, who is involved in the research. In addition to establishing safety, the current phase 1 trial will explore four different doses of the study
Wednesday, July 7, 2010
Tyrosine Kinase inhibitor shows promise for AMD treatment
A new study finds that inhibition of CXCR4 may be useful in preventing neovascularization but does not appear to have an effect on already established angiogenesis, whereas a multiple receptor tyrosine kinase inhibitor (SU14813) reduced the size of previously formed lesions.
Endothelial precursor cells (EPCs) derived from hematopoietic stem cells (HSCs) have been shown to contribute to choroidal neovascularization (CNV) by signaling through the SDF-1 and its receptor, known as CXCR4. Hematopoietic stem cells are implicated in the formation of new pathologic vessels observed in wet AMD. Recruitment of endothelial precursor cells to the site of neovascularization is mediated, in part, by the chemokine SDF-1, and its receptor, CXCR4. CXCR4 is a G-protein-coupled receptor found on lymphocytes, monocytes, hematopoietic, endothelial progenitor cells, and mature endothelial cells.
Methods and Results
CNV in rats was generated by focal rupture of Bruch's membrane with an 810-nm diode laser. In the prevention mode, a CXCR4 antagonist (AMD3100) was delivered via an osmotic pump 1 day after laser induction. In the intervention mode, AMD3100 delivery commenced 14 days after laser induction. Inhibition of CXCR4 was determined through leukocyte and SDF-1 actin polymerization blood biomarker assays. Leakage was assessed by fluorescein angiography, and CNV lesion size was quantified after isolectin B4 endothelial cell staining. SU14813, an anti-VEGFR, PDGFR-beta, KIT, and FLT3 inhibitor, was also assessed in an intervention study protocol.
Related News
CCR3 is a target for AMD diagnosis and therapy
Integrin α5β1 inhibitor JSM6427 combats CNV in animal study
Stem cells show promise to restore vision
Inhibition of CXCR4 was demonstrated by an increase in the number of blood leukocytes, and diminished SDF-1 induced actin polymerization in whole blood. CNV leakage and neovascularization were inhibited when the dose regimen was initiated 1 day after laser-induced CNV induction. AMD3100 did not show efficacy when administered 14 days after lasering. Treatment with SU14813 significantly decreased CNV leakage and lesion size in an intervention modality.
Discussion and Conclusions
In this study, CXCR4 inhibition was efficacious in the prevention of CNV, but failed to reduce choroidal leakage and angiogenesis in the intervention modality. This finding suggests that therapies targeting the SDF-1/CXCR4 axis may be beneficial in blocking the induction of ocular neoangiogenesis, but are unlikely to reduce already established angiogenesis.
There is strong evidence that CXCR4 inhibition disrupts the recruitment of endothelial precursor cells (EPCs) to sites of angiogenesis, most likely the major mechanism leading to efficacy in the prevention model.
In addition to suppressing CNV, CXCR4 inhibition reduced choroidal vascular leakage in the prevention modality (but not in the intervention modality). It is not known whether CXCR4 inhibition decreases leakage directly or as a secondary effect of the reduction of the angiogenic vessel area.
The observation that CXCR4 inhibition did not decrease choroidal leakage or angiogenic lesion size in the intervention modality suggests that after a 2-week generation of laser-induced CNV, there is limited, if any, contribution of EPC cells to the already established vessels
A multiple receptor tyrosine kinase (RTK) inhibitor may still be an effective monotherapy, as SU14813 reduced the size of previously formed lesions. In treatment mode, both leakage and angiogenesis decreased even after the pathologic effect was given 14 days to fully establish before drug intervention. This study suggests that blockade of the VEGF receptor is an effective alternative method of inhibiting the VEGF pathway compared to conventional anti-VEGF strategies.
SU14813 is a small molecule with broad target RTK selectivity, inhibiting the VEGF receptor (VEGFR), PDGFR-β, KIT, and FLT3. Although the primary mechanism that reduces preexisting angiogenesis and leakage is the blockade of the central VEGF pathway, the additional inhibition of PDGFR-β may augment efficacy in this model over single anti-VEGFR agents.
The investigators conclude that inhibition of CXCR4 may be useful in preventing neovascularization but does not appear to have an effect on already established angiogenesis. A multiple receptor tyrosine kinase inhibitor (SU14813) approach shows promise for the treatment of wet age-related macular degeneration.
Endothelial precursor cells (EPCs) derived from hematopoietic stem cells (HSCs) have been shown to contribute to choroidal neovascularization (CNV) by signaling through the SDF-1 and its receptor, known as CXCR4. Hematopoietic stem cells are implicated in the formation of new pathologic vessels observed in wet AMD. Recruitment of endothelial precursor cells to the site of neovascularization is mediated, in part, by the chemokine SDF-1, and its receptor, CXCR4. CXCR4 is a G-protein-coupled receptor found on lymphocytes, monocytes, hematopoietic, endothelial progenitor cells, and mature endothelial cells.
Methods and Results
CNV in rats was generated by focal rupture of Bruch's membrane with an 810-nm diode laser. In the prevention mode, a CXCR4 antagonist (AMD3100) was delivered via an osmotic pump 1 day after laser induction. In the intervention mode, AMD3100 delivery commenced 14 days after laser induction. Inhibition of CXCR4 was determined through leukocyte and SDF-1 actin polymerization blood biomarker assays. Leakage was assessed by fluorescein angiography, and CNV lesion size was quantified after isolectin B4 endothelial cell staining. SU14813, an anti-VEGFR, PDGFR-beta, KIT, and FLT3 inhibitor, was also assessed in an intervention study protocol.
Related News
CCR3 is a target for AMD diagnosis and therapy
Integrin α5β1 inhibitor JSM6427 combats CNV in animal study
Stem cells show promise to restore vision
Inhibition of CXCR4 was demonstrated by an increase in the number of blood leukocytes, and diminished SDF-1 induced actin polymerization in whole blood. CNV leakage and neovascularization were inhibited when the dose regimen was initiated 1 day after laser-induced CNV induction. AMD3100 did not show efficacy when administered 14 days after lasering. Treatment with SU14813 significantly decreased CNV leakage and lesion size in an intervention modality.
Discussion and Conclusions
In this study, CXCR4 inhibition was efficacious in the prevention of CNV, but failed to reduce choroidal leakage and angiogenesis in the intervention modality. This finding suggests that therapies targeting the SDF-1/CXCR4 axis may be beneficial in blocking the induction of ocular neoangiogenesis, but are unlikely to reduce already established angiogenesis.
There is strong evidence that CXCR4 inhibition disrupts the recruitment of endothelial precursor cells (EPCs) to sites of angiogenesis, most likely the major mechanism leading to efficacy in the prevention model.
In addition to suppressing CNV, CXCR4 inhibition reduced choroidal vascular leakage in the prevention modality (but not in the intervention modality). It is not known whether CXCR4 inhibition decreases leakage directly or as a secondary effect of the reduction of the angiogenic vessel area.
The observation that CXCR4 inhibition did not decrease choroidal leakage or angiogenic lesion size in the intervention modality suggests that after a 2-week generation of laser-induced CNV, there is limited, if any, contribution of EPC cells to the already established vessels
A multiple receptor tyrosine kinase (RTK) inhibitor may still be an effective monotherapy, as SU14813 reduced the size of previously formed lesions. In treatment mode, both leakage and angiogenesis decreased even after the pathologic effect was given 14 days to fully establish before drug intervention. This study suggests that blockade of the VEGF receptor is an effective alternative method of inhibiting the VEGF pathway compared to conventional anti-VEGF strategies.
SU14813 is a small molecule with broad target RTK selectivity, inhibiting the VEGF receptor (VEGFR), PDGFR-β, KIT, and FLT3. Although the primary mechanism that reduces preexisting angiogenesis and leakage is the blockade of the central VEGF pathway, the additional inhibition of PDGFR-β may augment efficacy in this model over single anti-VEGFR agents.
The investigators conclude that inhibition of CXCR4 may be useful in preventing neovascularization but does not appear to have an effect on already established angiogenesis. A multiple receptor tyrosine kinase inhibitor (SU14813) approach shows promise for the treatment of wet age-related macular degeneration.
Wednesday, June 30, 2010
Finding Macular Degeneration Treatments
Finding macular degeneration treatment s. Vision problems due to the onset of macular degeneration are quite prevalent, especially in the elderly. Macular degeneration occurs when the macula, located in the central portion of the retina in the eye, becomes weakened or damaged. The result is a loss of central vision. Central vision is used to read and drive, so it is crucial to save as much of a patient’s vision as possible as soon as possible. Although this medical condition has no cure at this time, there are some promising new macular degeneration treatments that have shown to alleviate and slow down some of the symptoms of age-related macular degeneration.
There is a range of vision loss that can occur depending on the severity and type of age-related macular degeneration a patient has. Because it affects the macula located in the center of the retina, a patient’s peripheral vision is usually not adversely affected by the condition. With the onset of the condition, a patient’s vision might still be quite good, but the situation can worsen over time. There are two different types of age-related macular degeneration that often result in the greatest loss of central vision, and they are called wet and dry. The dry form of advanced macular degeneration is caused by the reduction of the rods and cones located in the retina, while wet advanced macular degeneration occurs due to leakage of excessive blood vessels and the resulting scarring under the macula.
One thing that retinal specialists might tell their patients with macular degeneration is to take certain vitamins as part of a spectrum of macular degeneration treatment s. Patients in the initial onset stages of this condition sometimes benefit from taking vitamins C, E, zinc, lutein, zeaxanthin and eating foods that are high in beta-carotenes, such as dark green leafy vegetables, corn and peas.
Another macular degeneration treatment can be found in cholesterol reducing drugs. People in the early stages of this medical condition often develop drusen, or yellow deposits, in the macula. The development and increase in the number of drusen seems to be related to the patient’s cholesterol level, with drusen more prevalent in those with higher cholesterol. Medications, such as statins, which reduce cholesterol, and aspirin, which reduces inflammation, may have a significant impact on reducing the size and number of drusen in the macula and thus lessen the chances of someone developing age-related macular degeneration.
A couple of wet advanced macular degeneration treatments, Macugen and Lucentis, have been approved by the FDA. Macugen is useful because it helps to reduce the number of excessive blood vessels that can grow under the retina. These can become inflamed and eventually burst, causing vision problems. Lucentis also reduces the growth of too many blood vessels. Lucentis is administered as an injection under the eye, and offers a great new treatment option for some patients with these kinds of vision problems.
The future is looking brighter with these emerging new macular degeneration treatments.
Susan Slobac has had a parent diagnosed with macular degeneration. She has had experience in macular degeneration treatment. In this article, she discusses macular degeneration risk factors.
For more information follow us at www.maculardegenerationassociation.org
There is a range of vision loss that can occur depending on the severity and type of age-related macular degeneration a patient has. Because it affects the macula located in the center of the retina, a patient’s peripheral vision is usually not adversely affected by the condition. With the onset of the condition, a patient’s vision might still be quite good, but the situation can worsen over time. There are two different types of age-related macular degeneration that often result in the greatest loss of central vision, and they are called wet and dry. The dry form of advanced macular degeneration is caused by the reduction of the rods and cones located in the retina, while wet advanced macular degeneration occurs due to leakage of excessive blood vessels and the resulting scarring under the macula.
One thing that retinal specialists might tell their patients with macular degeneration is to take certain vitamins as part of a spectrum of macular degeneration treatment s. Patients in the initial onset stages of this condition sometimes benefit from taking vitamins C, E, zinc, lutein, zeaxanthin and eating foods that are high in beta-carotenes, such as dark green leafy vegetables, corn and peas.
Another macular degeneration treatment can be found in cholesterol reducing drugs. People in the early stages of this medical condition often develop drusen, or yellow deposits, in the macula. The development and increase in the number of drusen seems to be related to the patient’s cholesterol level, with drusen more prevalent in those with higher cholesterol. Medications, such as statins, which reduce cholesterol, and aspirin, which reduces inflammation, may have a significant impact on reducing the size and number of drusen in the macula and thus lessen the chances of someone developing age-related macular degeneration.
A couple of wet advanced macular degeneration treatments, Macugen and Lucentis, have been approved by the FDA. Macugen is useful because it helps to reduce the number of excessive blood vessels that can grow under the retina. These can become inflamed and eventually burst, causing vision problems. Lucentis also reduces the growth of too many blood vessels. Lucentis is administered as an injection under the eye, and offers a great new treatment option for some patients with these kinds of vision problems.
The future is looking brighter with these emerging new macular degeneration treatments.
Susan Slobac has had a parent diagnosed with macular degeneration. She has had experience in macular degeneration treatment. In this article, she discusses macular degeneration risk factors.
For more information follow us at www.maculardegenerationassociation.org
Thursday, June 10, 2010
Wider access to drug to prevent and reverse eye damage
By: Staff Writer
Manitobans now have wider access to a drug to prevent and reverse eye damage, Health Minister Theresa Oswald said Wednesday.
The drug Lucentis is now available through doctors' offices to treat wet macular degeneration.
Last March the province said Manitoba Health would cover Lucentis treatment though the Misericordia Eye Centre of Excellence as of June 1.
At that time the province said it wanted to expand patient access to Lucentis through other retinal specialists' offices.
Oswald said Lucentis is now accessible through doctors' offices ahead of schedule.
Wet macular degeneration is a disease that can impair vision and cause blindness.
Lucentis has been available at no cost to Manitobans with wet macular degeneration since June 1 through the Misericordia and Manitoba retinal specialists.
Manitoba Health says up to 1,000 patients could benefit from this new program annually.
Manitobans now have wider access to a drug to prevent and reverse eye damage, Health Minister Theresa Oswald said Wednesday.
The drug Lucentis is now available through doctors' offices to treat wet macular degeneration.
Last March the province said Manitoba Health would cover Lucentis treatment though the Misericordia Eye Centre of Excellence as of June 1.
At that time the province said it wanted to expand patient access to Lucentis through other retinal specialists' offices.
Oswald said Lucentis is now accessible through doctors' offices ahead of schedule.
Wet macular degeneration is a disease that can impair vision and cause blindness.
Lucentis has been available at no cost to Manitobans with wet macular degeneration since June 1 through the Misericordia and Manitoba retinal specialists.
Manitoba Health says up to 1,000 patients could benefit from this new program annually.
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