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.
Showing posts with label blurry vision. Show all posts
Showing posts with label blurry vision. Show all posts
Sunday, January 23, 2011
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.
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.
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.
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.
Saturday, September 18, 2010
Advanced Cell Technology Obtains Broad Patent covering use of Stem Cell
Sep 14, 2010 by Advanced Cell Techno;ogy
Advanced Cell Technology, Inc. ("ACT"; OTCBB: ACTC), a leader in the field of regenerative medicine, announced today that it will be issued U.S. Patent Numbers 7,795,025 and 7,794,704 on Tuesday, September 14th, which continue to extend the company's patent portfolio covering its retinal pigment epithelial (RPE) cell programs. In particular, the claims that will issue in patent number 7,794,704 broadly cover methods for treating retinal degeneration using human RPE cells differentiated from human embryonic stem cells (hESCs). Issuing with 68 claims, this patent covers methods of treatment with hESC-derived RPE cells that includes, but is not limited to, Stargardt's disease, retinitis pigmentosa, and macular degeneration. The 41 claims issuing in US Patent 7,795,025 contribute to the development of the company's protection of the processes for manufacturing RPE cells from human ES cells. The patent covers fundamental methods for generating transplantable cells for treatment of human patients.
"Another wonderful milestone for ACT! These patents continue the recognition of the inventions and innovations resulting from our scientific team's ongoing research, and further protects the platform technology underlying our RPE program, one of our key therapeutic programs," said William M. Caldwell IV, ACT's Chairman and CEO. "A valuable addition to our strong intellectual property portfolio, these patents should help position ACT as the dominant player in this potentially very large market. Our RPE technology is safe and scalable, and has tremendous potential for treating some 200 or more diseases of the retina."
"ACT is developing first-in-class treatments for degenerative disorders of the retina," said Robert Lanza, M.D., ACT's Chief Scientific Officer. "The use of RPE cells created from human embryonic stem cells should open the door to potential treatments for many diseases of the retina that impact sight. According to the World Health Organization, macular degeneration alone is known to affect 30-40 million people worldwide, and this represents only a handful of the 200 diseases that may be treated using our RPE cells. We have worked hard to develop an efficient method for producing a renewable source of transplantable RPE cells that can be used to target diseases such as Stargardt's Disease and Age-related Macular Degeneration. For many of these patients there are no available treatments. We have demonstrated that our stem cell-derived RPE cells can rescue visual function in animals that otherwise would have gone blind. We are looking forward to starting our clinical trials with the hope that these cells will be similarly efficacious in patients."
"We believe that these patents are especially important as they extend the company's patent coverage of the scalable manufacturing of human RPE cells for therapeutic use, which are core to our technology and product portfolio," continued Mr. Caldwell. "This IP further expands our patent estate with respect to protecting the use of RPE cells in a wide range of treatments, offering additional validation of the strength and breadth of our patent portfolio. This development also dovetails nicely with the prospect of initiating our human clinical trial for our RPE program. We are optimistic that the methods-of-treatments and the culturing processes covered by these two new patents, along with the Company's proprietary detection technique for final product release, will establish a formidable barrier to entry for any potential competitors. Once we have begun to treat Stargardt patients, we plan to initiate another clinical trial relating to the use of RPE cells in the treatment of dry Age-Related Macular Degeneration (AMD). At present there is no approved treatment for dry AMD, despite the fact that it represents a $20-30 billion potential market."
ACT's Single Blastomere technology used for isolating hESCs does not require the destruction of embryos. The RPE and other hESC-derived cells the company intends to produce for clinical use all begin with these "embryo-safe" stem cells. ACT does not rely on government funding for any of its research or development efforts, and accordingly has not been impacted by the recent court injunction against federal funding of hESC research. Nevertheless, the company's hESC lines and cells made for those lines (such as RPE cells) should fall outside the scope of the court order. While the injunction has been stayed, it is widely believed that this is only a temporary reprieve, with a permanent injunction a real possibility perhaps as early as the end of this month. Should that come to pass, ACT stands ready to offer its human stem cell lines to the research community, pending their approval by the National Institutes of Health (NIH).
About Advanced Cell Technology, Inc.
Advanced Cell Technology, Inc. is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.
Forward-Looking Statements
Statements in this news release regarding future financial and operating results, future growth in research and development programs, potential applications of our technology, opportunities for the company and any other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any statements that are not statements of historical fact (including statements containing the words "will," "believes," "plans," "anticipates," "broad," "expects," "estimates," and similar expressions) should also be considered to be forward-looking statements. There are a number of important factors that could cause actual results or events to differ materially from those indicated by such forward-looking statements, including: limited operating history, need for future capital, risks inherent in the development and commercialization of potential products, scope and enforceability of our intellectual property, and economic conditions generally. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in the company's periodic reports, including the report on Form 10-K for the year ended December 31, 2009.
Forward-looking statements are based on the beliefs, opinions, and expectations of the company's management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. Forward-looking statements are based on the beliefs, opinions, and expectations of the company's management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change.
Advanced Cell Technology, Inc. ("ACT"; OTCBB: ACTC), a leader in the field of regenerative medicine, announced today that it will be issued U.S. Patent Numbers 7,795,025 and 7,794,704 on Tuesday, September 14th, which continue to extend the company's patent portfolio covering its retinal pigment epithelial (RPE) cell programs. In particular, the claims that will issue in patent number 7,794,704 broadly cover methods for treating retinal degeneration using human RPE cells differentiated from human embryonic stem cells (hESCs). Issuing with 68 claims, this patent covers methods of treatment with hESC-derived RPE cells that includes, but is not limited to, Stargardt's disease, retinitis pigmentosa, and macular degeneration. The 41 claims issuing in US Patent 7,795,025 contribute to the development of the company's protection of the processes for manufacturing RPE cells from human ES cells. The patent covers fundamental methods for generating transplantable cells for treatment of human patients.
"Another wonderful milestone for ACT! These patents continue the recognition of the inventions and innovations resulting from our scientific team's ongoing research, and further protects the platform technology underlying our RPE program, one of our key therapeutic programs," said William M. Caldwell IV, ACT's Chairman and CEO. "A valuable addition to our strong intellectual property portfolio, these patents should help position ACT as the dominant player in this potentially very large market. Our RPE technology is safe and scalable, and has tremendous potential for treating some 200 or more diseases of the retina."
"ACT is developing first-in-class treatments for degenerative disorders of the retina," said Robert Lanza, M.D., ACT's Chief Scientific Officer. "The use of RPE cells created from human embryonic stem cells should open the door to potential treatments for many diseases of the retina that impact sight. According to the World Health Organization, macular degeneration alone is known to affect 30-40 million people worldwide, and this represents only a handful of the 200 diseases that may be treated using our RPE cells. We have worked hard to develop an efficient method for producing a renewable source of transplantable RPE cells that can be used to target diseases such as Stargardt's Disease and Age-related Macular Degeneration. For many of these patients there are no available treatments. We have demonstrated that our stem cell-derived RPE cells can rescue visual function in animals that otherwise would have gone blind. We are looking forward to starting our clinical trials with the hope that these cells will be similarly efficacious in patients."
"We believe that these patents are especially important as they extend the company's patent coverage of the scalable manufacturing of human RPE cells for therapeutic use, which are core to our technology and product portfolio," continued Mr. Caldwell. "This IP further expands our patent estate with respect to protecting the use of RPE cells in a wide range of treatments, offering additional validation of the strength and breadth of our patent portfolio. This development also dovetails nicely with the prospect of initiating our human clinical trial for our RPE program. We are optimistic that the methods-of-treatments and the culturing processes covered by these two new patents, along with the Company's proprietary detection technique for final product release, will establish a formidable barrier to entry for any potential competitors. Once we have begun to treat Stargardt patients, we plan to initiate another clinical trial relating to the use of RPE cells in the treatment of dry Age-Related Macular Degeneration (AMD). At present there is no approved treatment for dry AMD, despite the fact that it represents a $20-30 billion potential market."
ACT's Single Blastomere technology used for isolating hESCs does not require the destruction of embryos. The RPE and other hESC-derived cells the company intends to produce for clinical use all begin with these "embryo-safe" stem cells. ACT does not rely on government funding for any of its research or development efforts, and accordingly has not been impacted by the recent court injunction against federal funding of hESC research. Nevertheless, the company's hESC lines and cells made for those lines (such as RPE cells) should fall outside the scope of the court order. While the injunction has been stayed, it is widely believed that this is only a temporary reprieve, with a permanent injunction a real possibility perhaps as early as the end of this month. Should that come to pass, ACT stands ready to offer its human stem cell lines to the research community, pending their approval by the National Institutes of Health (NIH).
About Advanced Cell Technology, Inc.
Advanced Cell Technology, Inc. is a biotechnology company applying cellular technology in the field of regenerative medicine. For more information, visit http://www.advancedcell.com.
Forward-Looking Statements
Statements in this news release regarding future financial and operating results, future growth in research and development programs, potential applications of our technology, opportunities for the company and any other statements about the future expectations, beliefs, goals, plans, or prospects expressed by management constitute forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995. Any statements that are not statements of historical fact (including statements containing the words "will," "believes," "plans," "anticipates," "broad," "expects," "estimates," and similar expressions) should also be considered to be forward-looking statements. There are a number of important factors that could cause actual results or events to differ materially from those indicated by such forward-looking statements, including: limited operating history, need for future capital, risks inherent in the development and commercialization of potential products, scope and enforceability of our intellectual property, and economic conditions generally. Additional information on potential factors that could affect our results and other risks and uncertainties are detailed from time to time in the company's periodic reports, including the report on Form 10-K for the year ended December 31, 2009.
Forward-looking statements are based on the beliefs, opinions, and expectations of the company's management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change. Forward-looking statements are based on the beliefs, opinions, and expectations of the company's management at the time they are made, and the company does not assume any obligation to update its forward-looking statements if those beliefs, opinions, expectations, or other circumstances should change.
Sunday, September 12, 2010
How to prevent age-related macular degeneration
by Dr Pandula Siribaddana
Age Related Macular Degeneration or ARMD is a common condition seen in the elderly population and can be named as one of the commonest causes of visual loss among the same age group. The condition is characterized by the gradual loss of central vision and could be recognized as having two major categories.
In one form, which is the ‘dry’ macular degeneration, the retina and the layer below in the back of the eye would be separated by cellular debris and in the second form, which is the ‘wet’ macular degeneration, the two layers will be separated by enlarging blood vessels under the retina. In both instances, the peripheral vision would be spared and therefore, these individuals would be able to carry out their daily activities, although the functions such as reading would be impaired to a significant extent.
How to prevent ARMD in the elderly?
The prevention strategies related to ARMD would include avoiding the risk factors which would cause the condition in the first place. Therefore, following prevention strategies can be named as the most useful in order to achieve better vision in the elderly age.
Control blood sugar levels
This has shown to have an influence in the manifestation of macular degeneration and since it is prevalent abundantly, adhering to good glycaemic control would be essential to reduce the disease burden of ARMD.
Avoid smoking
Among the many influences it makes on health, macular degeneration is one and therefore its avoidance would greatly help susceptible individuals to maintain better visual health. According to statistics, there seems to be a threefold risk among the smokers than in non-smokers to develop ARMD during the elderly life.
Control hypertension and cardiovascular diseases
Researchers have identified these two as influencing the occurrence of macular degeneration and controlling of the same would reduce the risk of ARMD in susceptible individuals.
Avoid direct sun light
Sun light, particularly the blue light in the sun’s rays, have shown to influence the functioning of the retina and thus can lead to the development of ARMD. Therefore, using special eye glasses and avoiding such exposure would be recommended for people whom are constantly at risk of being exposed.
Include carotenes in the diet
Carotenes containing foods or else supplements have shown to be effective to a certain extent in reducing the risk of macular degeneration and therefore steps should be taken to include such foods and to take a balanced diet as much as possible.
Add omega 3 fatty acids
Similar to carotenes, omega 3 fatty acids are suggested as being supportive in the prevention of ARMD and should be included in the diets of all ages.
Lastly, due to the fact that there are other factors which are not modifiable and may lead to the development of ARMD, it is always best to screen and initiate treatment as early as possible in order to prevent progression of the disease and to avoid the occurrence of complete blindness.
Age Related Macular Degeneration or ARMD is a common condition seen in the elderly population and can be named as one of the commonest causes of visual loss among the same age group. The condition is characterized by the gradual loss of central vision and could be recognized as having two major categories.
In one form, which is the ‘dry’ macular degeneration, the retina and the layer below in the back of the eye would be separated by cellular debris and in the second form, which is the ‘wet’ macular degeneration, the two layers will be separated by enlarging blood vessels under the retina. In both instances, the peripheral vision would be spared and therefore, these individuals would be able to carry out their daily activities, although the functions such as reading would be impaired to a significant extent.
How to prevent ARMD in the elderly?
The prevention strategies related to ARMD would include avoiding the risk factors which would cause the condition in the first place. Therefore, following prevention strategies can be named as the most useful in order to achieve better vision in the elderly age.
Control blood sugar levels
This has shown to have an influence in the manifestation of macular degeneration and since it is prevalent abundantly, adhering to good glycaemic control would be essential to reduce the disease burden of ARMD.
Avoid smoking
Among the many influences it makes on health, macular degeneration is one and therefore its avoidance would greatly help susceptible individuals to maintain better visual health. According to statistics, there seems to be a threefold risk among the smokers than in non-smokers to develop ARMD during the elderly life.
Control hypertension and cardiovascular diseases
Researchers have identified these two as influencing the occurrence of macular degeneration and controlling of the same would reduce the risk of ARMD in susceptible individuals.
Avoid direct sun light
Sun light, particularly the blue light in the sun’s rays, have shown to influence the functioning of the retina and thus can lead to the development of ARMD. Therefore, using special eye glasses and avoiding such exposure would be recommended for people whom are constantly at risk of being exposed.
Include carotenes in the diet
Carotenes containing foods or else supplements have shown to be effective to a certain extent in reducing the risk of macular degeneration and therefore steps should be taken to include such foods and to take a balanced diet as much as possible.
Add omega 3 fatty acids
Similar to carotenes, omega 3 fatty acids are suggested as being supportive in the prevention of ARMD and should be included in the diets of all ages.
Lastly, due to the fact that there are other factors which are not modifiable and may lead to the development of ARMD, it is always best to screen and initiate treatment as early as possible in order to prevent progression of the disease and to avoid the occurrence of complete blindness.
Monday, August 23, 2010
Macular Degeneration Surgery
By Joven Villanueva
While the quest in searching for the cure of macular degeneration is on going. Many national eye centers are investigating new ways to treat the said illness. There are different options in managing macular degeneration as the illness has two types. The wet form which usually results to loss of vision due to no reliable treatment yet to be developed and the dry form accounting 90% of cases can still be managed and controlled if diagnosed at an early stage and by eating the right food rich in vitamins A, C, E and other supplements such as zeaxanthine and zinc - proven to be effective in slowing down the disease
Here are some optional treatments available for patients having the wet form of macular degeneration. First is Photodynamic therapy which uses a combination of both cold laser and light-sensitive drug destroying abnormal blood vessels as the drug travels to the unwanted vessels after it was injected from the arm. Another option is Laser therapy where high energy lights are used to destroy abnormal growing blood vessels.
The Cole eye institute is conducting experimental treatments such as a surgery to remove abnormal blood vessels and blood. A genetically engineered enzyme is used by the surgeon to dissolve blood clots under the macula. Another procedure is called Macular translocation.This is performed using a laser therapy to treat abnormal blood vessel. To prevent the formation of scar tissue and damage to retina, the surgeon rotates the retina in a healthy area.
The healing process may take three to six weeks. The doctor may request for an angiogram after the macular surgery to make sure that there are no additional blood leakage in the area. An additional laser treatment maybe performed if a problem was observed.
Macular degeneration is a medical condition resulting to loss of vision making it difficult to read and recognize faces. To better understand the patient's condition, print out some letters six inches high and try to identify them while looking it at straight ahead. Hold the paper slightly to the side. This visual impairment does not lead to total blindness and in most cases some vision remains.
This disease mostly affects older and adults 50 years old and above. In a recent study for macular degeneration it was found out that those patients aging sixty six to seventy four suffer from this illness. Mostly women are prone to macular degeneration compare to men and smokers of any gender are also part of the growing list as tobacco increase the risk in three folds due to the toxic effects in retina. It is even 50% risky for those who have relatives with muscular degeneration to develop the illness compare to those who doesn't have with only 12% probability. Caucasians are more prone to develop macular degeneration compare to other races.
Other than age and family history, there are factors that cause macular degeneration. These includes hypertension or commonly known as high blood pressure, obesity, and high fat intake.
Ophthalmologists diagnose macular degeneration by looking at the abnormal vessels under the retina. A dye is injected in the arm of the patient where pictures are taken by a special camera until it reaches the eye. Any changes in the retina as shown from the photographs taken will serve as a guide for treatment.
While the quest in searching for the cure of macular degeneration is on going. Many national eye centers are investigating new ways to treat the said illness. There are different options in managing macular degeneration as the illness has two types. The wet form which usually results to loss of vision due to no reliable treatment yet to be developed and the dry form accounting 90% of cases can still be managed and controlled if diagnosed at an early stage and by eating the right food rich in vitamins A, C, E and other supplements such as zeaxanthine and zinc - proven to be effective in slowing down the disease
Here are some optional treatments available for patients having the wet form of macular degeneration. First is Photodynamic therapy which uses a combination of both cold laser and light-sensitive drug destroying abnormal blood vessels as the drug travels to the unwanted vessels after it was injected from the arm. Another option is Laser therapy where high energy lights are used to destroy abnormal growing blood vessels.
The Cole eye institute is conducting experimental treatments such as a surgery to remove abnormal blood vessels and blood. A genetically engineered enzyme is used by the surgeon to dissolve blood clots under the macula. Another procedure is called Macular translocation.This is performed using a laser therapy to treat abnormal blood vessel. To prevent the formation of scar tissue and damage to retina, the surgeon rotates the retina in a healthy area.
The healing process may take three to six weeks. The doctor may request for an angiogram after the macular surgery to make sure that there are no additional blood leakage in the area. An additional laser treatment maybe performed if a problem was observed.
Macular degeneration is a medical condition resulting to loss of vision making it difficult to read and recognize faces. To better understand the patient's condition, print out some letters six inches high and try to identify them while looking it at straight ahead. Hold the paper slightly to the side. This visual impairment does not lead to total blindness and in most cases some vision remains.
This disease mostly affects older and adults 50 years old and above. In a recent study for macular degeneration it was found out that those patients aging sixty six to seventy four suffer from this illness. Mostly women are prone to macular degeneration compare to men and smokers of any gender are also part of the growing list as tobacco increase the risk in three folds due to the toxic effects in retina. It is even 50% risky for those who have relatives with muscular degeneration to develop the illness compare to those who doesn't have with only 12% probability. Caucasians are more prone to develop macular degeneration compare to other races.
Other than age and family history, there are factors that cause macular degeneration. These includes hypertension or commonly known as high blood pressure, obesity, and high fat intake.
Ophthalmologists diagnose macular degeneration by looking at the abnormal vessels under the retina. A dye is injected in the arm of the patient where pictures are taken by a special camera until it reaches the eye. Any changes in the retina as shown from the photographs taken will serve as a guide for treatment.
Monday, July 26, 2010
Commencement of CABERNET clinical trial
NeoVista, Inc announced the official commencement of the CABERNET (Cnv Secondary Amd Treated with BEta RadiatioN Epiretinal Therapy) clinical trial for the treatment of subfoveal choroidal neovascularization associated with wet age-related macular degeneration (AMD). Neovascular AMD is the leading cause of irreparable blindness in the elderly population, afflicting over 200,000 individuals each year in the U.S.
Dr. Nelson Sabates, Professor and Chairman, Department of Ophthalmology, University of Missouri-Kansas City (UMKC)/Truman Medical Centers and Director of Vision Research Center, University of Missouri-Kansas City at Truman Medical Centers performed the procedure on the first patient enrolled in the CABERNET study. When asked for initial feedback on the procedure, Dr. Sabates commented, "The procedure was no different than performing a common vitrectomy and the Epi-Rad device allowed me to deliver a well focused dose of radiation to the lesion. Treating neovascular AMD using a multi-faceted approach like the use of radiation and anti-VEGF therapy may well be the next frontier in combating this sight threatening disease."
The CABERNET clinical trial will involve clinical sites in the United States, Europe, Israel, and South America. The CABERNET trial protocol is divided into two treatment arms - investigational and control.
The investigational treatment arm consists of concomitant delivery of Beta radiation, via the proprietary NeoVista technology (Epi-Rad90™), and an FDA approved anti-VEGF agent. The investigational treatment is administered during an outpatient surgical procedure and delivers Beta radiation directly to the area of the retina that has been compromised by the disease. An injection of the anti-VEGF agent is administered at the time of surgery with one additional injection administered 30 days after surgery. The control arm is utilizing the FDA approved anti-VEGF agent alone.
The surgery was performed in collaboration with, Saint Lukes Hospital in Kansas City. Dr. Terry J. Wall, J.D., M.D. of the Saint Lukes Cancer Institute was the attending radiation oncologist involved with the procedure.
"This is a very good day for NeoVista employees and the investors who are supporting our work," stated John N. Hendrick, President and CEO of NeoVista. "More importantly, it is a potential harbinger of hope for those suffering from wet AMD." We remain optimistic that our treatment approach will provide maximum benefit to this patient population."
Dr. Nelson Sabates, Professor and Chairman, Department of Ophthalmology, University of Missouri-Kansas City (UMKC)/Truman Medical Centers and Director of Vision Research Center, University of Missouri-Kansas City at Truman Medical Centers performed the procedure on the first patient enrolled in the CABERNET study. When asked for initial feedback on the procedure, Dr. Sabates commented, "The procedure was no different than performing a common vitrectomy and the Epi-Rad device allowed me to deliver a well focused dose of radiation to the lesion. Treating neovascular AMD using a multi-faceted approach like the use of radiation and anti-VEGF therapy may well be the next frontier in combating this sight threatening disease."
The CABERNET clinical trial will involve clinical sites in the United States, Europe, Israel, and South America. The CABERNET trial protocol is divided into two treatment arms - investigational and control.
The investigational treatment arm consists of concomitant delivery of Beta radiation, via the proprietary NeoVista technology (Epi-Rad90™), and an FDA approved anti-VEGF agent. The investigational treatment is administered during an outpatient surgical procedure and delivers Beta radiation directly to the area of the retina that has been compromised by the disease. An injection of the anti-VEGF agent is administered at the time of surgery with one additional injection administered 30 days after surgery. The control arm is utilizing the FDA approved anti-VEGF agent alone.
The surgery was performed in collaboration with, Saint Lukes Hospital in Kansas City. Dr. Terry J. Wall, J.D., M.D. of the Saint Lukes Cancer Institute was the attending radiation oncologist involved with the procedure.
"This is a very good day for NeoVista employees and the investors who are supporting our work," stated John N. Hendrick, President and CEO of NeoVista. "More importantly, it is a potential harbinger of hope for those suffering from wet AMD." We remain optimistic that our treatment approach will provide maximum benefit to this patient population."
Treatment for Cataracts/ other eye diseases
What is a cataract?
There is only one known treatment for cataracts - surgery! A cataract needs to be removed only when vision loss interferes with your everyday activities, or the things you like to do such as driving, reading, sewing, playing golf or watching TV . You and your eye care professional can make this decision together. Once you understand the benefits and risks of surgery, you can make an informed decision about whether cataract surgery is right for you. In most cases, delaying cataract surgery will not cause long-term damage to your eye or make the surgery more difficult. You do not have to rush into surgery.
Additionally, Medicare and most commercial insurance carriers require that best corrected vision be reduced to some level (often 20/50 visual acuity) before they will approve the surgery for payment.
Sometimes a cataract should be removed even if it does not cause problems with your vision. For example, a cataract should be removed if it prevents examination or treatment of another eye problem, such as age-related macular degeneration or diabetic retinopathy.
If you choose surgery, your optometrist will refer you to an ophthalmic surgeon to remove the cataract. This is a very definite advantage over choosing an eye surgeon out of the phone book or from your friends because your doctor knows firsthand the quality of the cataract surgery performed by local eye surgeons. Because they work with the eye surgeons and usually perform some or all of the post-op care they truly know where to refer you for the best possible outcome. If you have cataracts in both eyes that require surgery, the surgery will be performed on each eye at separate times, usually four to eight weeks apart.
As with any surgery, cataract surgery poses risks, such as infection and bleeding. Before cataract surgery, your doctor may ask you to temporarily stop taking certain medications that increase the risk of bleeding during surgery. After surgery, you must keep your eye clean, wash your hands before touching your eye, and use the prescribed medications to help minimize the risk of infection. Serious infection can result in loss of vision. Talk to your eye care professional about these risks. Make sure cataract surgery is right for you.
Cataract surgery slightly increases your risk of retinal detachment. Other eye disorders, such as high myopia (nearsightedness), can further increase your risk of retinal detachment after cataract surgery. One sign of a retinal detachment is a sudden increase in flashes or floaters. Floaters are little "cobwebs" or specks that seem to float about in your field of vision. If you notice a sudden increase in floaters or flashes, see an eye care professional immediately. A retinal detachment is a medical emergency. If necessary, go to an emergency service or hospital. Your eye should be examined by a retinal specialist as soon as possible. A retinal detachment causes no pain. Early treatment for retinal detachment often can prevent permanent loss of vision. The longer the retina stays detached, the less likely you will regain good vision once you are treated. Even if you are treated promptly, some vision may be lost.
There is only one known treatment for cataracts - surgery! A cataract needs to be removed only when vision loss interferes with your everyday activities, or the things you like to do such as driving, reading, sewing, playing golf or watching TV . You and your eye care professional can make this decision together. Once you understand the benefits and risks of surgery, you can make an informed decision about whether cataract surgery is right for you. In most cases, delaying cataract surgery will not cause long-term damage to your eye or make the surgery more difficult. You do not have to rush into surgery.
Additionally, Medicare and most commercial insurance carriers require that best corrected vision be reduced to some level (often 20/50 visual acuity) before they will approve the surgery for payment.
Sometimes a cataract should be removed even if it does not cause problems with your vision. For example, a cataract should be removed if it prevents examination or treatment of another eye problem, such as age-related macular degeneration or diabetic retinopathy.
If you choose surgery, your optometrist will refer you to an ophthalmic surgeon to remove the cataract. This is a very definite advantage over choosing an eye surgeon out of the phone book or from your friends because your doctor knows firsthand the quality of the cataract surgery performed by local eye surgeons. Because they work with the eye surgeons and usually perform some or all of the post-op care they truly know where to refer you for the best possible outcome. If you have cataracts in both eyes that require surgery, the surgery will be performed on each eye at separate times, usually four to eight weeks apart.
As with any surgery, cataract surgery poses risks, such as infection and bleeding. Before cataract surgery, your doctor may ask you to temporarily stop taking certain medications that increase the risk of bleeding during surgery. After surgery, you must keep your eye clean, wash your hands before touching your eye, and use the prescribed medications to help minimize the risk of infection. Serious infection can result in loss of vision. Talk to your eye care professional about these risks. Make sure cataract surgery is right for you.
Cataract surgery slightly increases your risk of retinal detachment. Other eye disorders, such as high myopia (nearsightedness), can further increase your risk of retinal detachment after cataract surgery. One sign of a retinal detachment is a sudden increase in flashes or floaters. Floaters are little "cobwebs" or specks that seem to float about in your field of vision. If you notice a sudden increase in floaters or flashes, see an eye care professional immediately. A retinal detachment is a medical emergency. If necessary, go to an emergency service or hospital. Your eye should be examined by a retinal specialist as soon as possible. A retinal detachment causes no pain. Early treatment for retinal detachment often can prevent permanent loss of vision. The longer the retina stays detached, the less likely you will regain good vision once you are treated. Even if you are treated promptly, some vision may be lost.
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.
Saturday, June 6, 2009
Exploiting Cortistatins' Essence
Simple analogs of a complex natural product may protect against loss of vision
Carmen Drahl
By making simplified versions of cortistatins, marine natural products that halt new blood vessel growth, researchers can treat excessive vessel growth in mice with macular degeneration. The analogs may inspire a new class of medications for the disease, which is a leading cause of vision loss.
Cortistatins A and J are potent blockers of angiogenesis, or new blood vessel growth, but the natural supply is scarce and chemical syntheses of the cortistatins haven't produced enough material for animal testing. Chemists Barbara Czakó, László Kürti, and E. J. Corey at Harvard University decided to study analogs instead.
"What distinguishes cortistatins are two basic groups at opposite ends of a steroidlike scaffold that are important for bioactivity," Corey says. His team incorporated those essential groups, a dimethylamino and an isoquinoline group, on opposite ends of an easy-to-build steroid and made refinements to optimize anti-angiogenic activity in cells. In collaboration with vascular biologists Akiko Mammoto and Donald E. Ingber of Harvard Medical School, they found that some of their compounds blocked angiogenesis in a mouse model of macular degeneration but did not show signs of toxicity in cellular assays (J. Am. Chem. Soc., DOI: 10.1021/ja902601e).
The most effective pharmaceutical treatment for macular degeneration is administered by injection into the eye, Corey notes. All of his team’s most potent analogs are water soluble and could lead to an eye-drop-based treatment, he says.
Chemist Samuel J. Danishefsky of Memorial Sloan-Kettering Cancer Center and Columbia University praised the work, saying that Corey's team “has increased the scope of the cortistatins by weaving them into a steroid setting which provided a doable terrain for chemical synthesis.”
"In terms of an exercise in blending intuition and rational discovery, this paper could emerge as a classic," Danishefsky adds.
Studies from other groups suggest that inhibitors of the particular angiogenesis pathway that the cortistatin analogs target may lead to side effects, cautions David A. Cheresh, who studies tumor angiogenesis at the University of California, San Diego. Nonetheless, the analogs "represent exciting new leads in the search for the next class of anti-angiogenic agents" and should be studied further, he adds.
Corey tells C&EN that the cortistatin analogs are effective in mice at very low doses of less than 1 mg and would also be locally administered. Therefore, the amount of drug that the rest of the body would see is likely to be essentially zero, vastly reducing the potential for side effects, he says.
In related work, independent teams led by Hiromasa Kiyota at Tohoku University in Japan and Phil S. Baran at Scripps Research Institute have tested simplified cortistatins in cells, but neither team has reported animal studies (Biosci. Biotechnol. Biochem. 2008, 72, 2992; Angew. Chem. Int. Ed., DOI: 10.1002/anie.200901116).
Carmen Drahl
By making simplified versions of cortistatins, marine natural products that halt new blood vessel growth, researchers can treat excessive vessel growth in mice with macular degeneration. The analogs may inspire a new class of medications for the disease, which is a leading cause of vision loss.
Cortistatins A and J are potent blockers of angiogenesis, or new blood vessel growth, but the natural supply is scarce and chemical syntheses of the cortistatins haven't produced enough material for animal testing. Chemists Barbara Czakó, László Kürti, and E. J. Corey at Harvard University decided to study analogs instead.
"What distinguishes cortistatins are two basic groups at opposite ends of a steroidlike scaffold that are important for bioactivity," Corey says. His team incorporated those essential groups, a dimethylamino and an isoquinoline group, on opposite ends of an easy-to-build steroid and made refinements to optimize anti-angiogenic activity in cells. In collaboration with vascular biologists Akiko Mammoto and Donald E. Ingber of Harvard Medical School, they found that some of their compounds blocked angiogenesis in a mouse model of macular degeneration but did not show signs of toxicity in cellular assays (J. Am. Chem. Soc., DOI: 10.1021/ja902601e).
The most effective pharmaceutical treatment for macular degeneration is administered by injection into the eye, Corey notes. All of his team’s most potent analogs are water soluble and could lead to an eye-drop-based treatment, he says.
Chemist Samuel J. Danishefsky of Memorial Sloan-Kettering Cancer Center and Columbia University praised the work, saying that Corey's team “has increased the scope of the cortistatins by weaving them into a steroid setting which provided a doable terrain for chemical synthesis.”
"In terms of an exercise in blending intuition and rational discovery, this paper could emerge as a classic," Danishefsky adds.
Studies from other groups suggest that inhibitors of the particular angiogenesis pathway that the cortistatin analogs target may lead to side effects, cautions David A. Cheresh, who studies tumor angiogenesis at the University of California, San Diego. Nonetheless, the analogs "represent exciting new leads in the search for the next class of anti-angiogenic agents" and should be studied further, he adds.
Corey tells C&EN that the cortistatin analogs are effective in mice at very low doses of less than 1 mg and would also be locally administered. Therefore, the amount of drug that the rest of the body would see is likely to be essentially zero, vastly reducing the potential for side effects, he says.
In related work, independent teams led by Hiromasa Kiyota at Tohoku University in Japan and Phil S. Baran at Scripps Research Institute have tested simplified cortistatins in cells, but neither team has reported animal studies (Biosci. Biotechnol. Biochem. 2008, 72, 2992; Angew. Chem. Int. Ed., DOI: 10.1002/anie.200901116).
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