Monday, December 14, 2009

What Is Goji Berries

Long a staple of Asian and holistic medicine, the most renowned properties of the Goji Berries is its antioxidant properties and it provide several benefits including increased energy and heightened immune function.

The weight loss properties of this natural ingredient have recently seen the fruit becoming popular stateside as well, especially among celebrities in Hollywood with the Goji Berry being featured on many television programs and in magazines.

Goji Berry Active have improved the many benefits of the Goji Berry by adding other natural ingredients to the Goji Berry Active Supplement designed to provide many other health benefits and increase its weight loss capabilities as well.

A complete all-natural supplement is the result and it is designed in pill form that can be easily taken with no powders or cumbersome ingredients to mix or measure. Just take as directed to help with immune function, weight loss and increasing energy levels.

What are they?

Other Names: Lycium barbarum, wolfberry, gou qi zi, Fructus lycii

Goji berries grow on an evergreen shrub found in subtropical and temperate regions in the Himalayas in Tibet, China and Mongolia. They are in the nightshade (Solonaceae) family.

Usually Goji berries are placed out to be dried They are shriveled red berries that look like red raisins.

Gojo berries are used by people for what purpose?

For 6,000 years, herbalists in China, India and Tibet have been using Goji berries to:

• protect the liver

• help eyesight

• improve sexual function and fertility

• strengthen the legs

• boost immune function

• improve circulation

• promote longevity

Goji berries are rich in antioxidants, particularly carotenoids such as beta-carotene and zeaxanthin. One of the key roles of zeaxanthin is to protect the retina of the eye by absorbing blue light and acting as an antioxidant. In fact, increased intake of foods containing zeathanthin may decrease the risk of developing age-related macular degeneration (AMD). For people over the age of 65, AMD is the number 1 cause of blindness and vision loss.

Goji juice has become popular as a health drink in recent years. Companies marketing goji juice often mention the unsupported claim that a man named Li Qing Yuen lived to be 252 years old after drinking goji berries everyday . Marketers also list extensive health benefits of goji juice, even though there are few published clinical trials in humans.

What research are being done on goji berries?

Goji has only been tested on humans in two published studies. A Chinese study published in 1994 in the Chinese Journal of Oncology found that 79 people with cancer responded better to treatment when goji was added to their regimen.

There have been several clinical studies that show that goji berry contains antioxidants and that goji extracts may lower cholesterol levels, reduce blood glucose and prevent the growth of cancer cells. However, even when taken as a juice or tea, it doesn’t necessary mean that goji will have the same benefits.

Although like the ones used in traditional Chinese medicine, goji berries are rather cheap, goji juice is not cheap. Considering that be as high as 50 US dollars~for a price running as high as 50 US dollars for a 32-ounce bottle of goji juice (about an 18-day supply)}, the evidence isn’t compelling enough at this time to justify the cost of goji juice.

Also, we don’t know the regular consumption of goji will cause any side effects, or whether treatments or medications will be interfered with.

What do goji berries taste like?

A mild tangy taste that is slightly sweet and sour, that is how we describe the taste of goji berries. They have a similar chewy texture and shape as raisins.

Common forms

In traditional Chinese medicine, goji berries can be made into liquid extracts, brewed into a tea, added to Chinese soup or eaten raw

Goji juice is also available, usually in 32-ounce bottles.

Goji berries have appeared in snack foods in North America. For example, Trader Joe’s, the health food store sells a goji berry trail mix.

Possible drug interactions

Anticoagulant drugs (commonly called “blood-thinners”), such as warfarin (Coumadin®) may interact with goji berries. There was one case report published in the journal Annals of Pharmacotherapy of a 61-year old woman who had an increased risk of bleeding, indicated by an elevated international normalized ratio (INR). She had been consuming 3-4 cups daily of goji berry tea. Her blood work returned to normal after she stopped drinking the goji berry tea.

For more information go to www.maculardegenerationassociation.org

Thursday, December 3, 2009

Can Heart Disease Treatments Combat Age-Related Macular Degeneration?

Can treatments that reduce risks for cardiovascular disease (CVD) also help combat age-related macular degeneration (AMD), an eye disease that affects millions of Americans? CVD and AMD share some risk factors–such as smoking, high blood pressure, and inflammation–and a recent study found that people who have early-stage AMD are more likely to develop heart disease. This month's Ophthalmology
, the journal of the American Academy of Ophthalmology, reports on how two heart disease treatments, low-dose aspirin and statin medications, may impact AMD risk and disease progression.

Low-dose Aspirin May Offer Mild Protection from AMD

Records for 39,421women enrolled in the 10-year Women's Health Study (WHS) were used to evaluate the impact of low-dose aspirin on AMD risk. None of the women had AMD at the study outset; they were randomly assigned to take low-dose aspirin (100 mg on alternate days) or a placebo. It is known that low-dose aspirin substantially reduces the risk of serious blood vessel blockage, so researchers reasoned it might affect blood vessels that may play a role in AMD. Aspirin's anti-inflammatory and anti-oxidant effects were also considered potentially relevant. The research was supported by the National Eye Institute.

"Although our study found no large benefit from low-dose aspirin, the possible modest protective effect we did find warrants further study," said lead researcher William G. Christen, ScD, of Brigham and Women's Hospital, Boston, MA. "If future studies confirm our findings, it could be important to make the public aware of this benefit," he added.

The risk of developing vision-impacting AMD was reduced by18 percent in women who took low-dose aspirin. During the 10 year study, 245 AMD cases developed, 111 in the aspirin group and 134 in the placebo group. "Vision impact" was defined as a reduction in visual acuity to 20/30 or worse due to AMD. Though not statistically significant, the WHS risk reduction is similar to the result of the only other large randomized trial on this question: the Physicians' Health Study I, which followed 22,071 men who took low-dose aspirin or a placebo for five years.

The primary aim of the WHS was to learn whether Vitamin E and low-dose aspirin would help prevent heart disease and cancer. The AMD study also found that women who were not taking multivitamins appeared to benefit more from low-dose aspirin than vitamin users.

Statins Do Not Stop Advanced AMD

In the largest study of statin use by advanced AMD patients to date, researchers followed 744 patients enrolled in the Complications of Age-Related Macular Degeneration Prevention Trial (CAPT) for five or six years. Statin drugs are primarily used to lower cholesterol in CVD patients, but they also affect mechanisms thought to impact AMD, including reduction of the inflammatory marker C-reactive protein. Earlier studies on statins' effects had been inconclusive. All patients from the CAPT cohort study were at risk for advanced AMD, but none had developed advanced "wet" or "dry" AMD at baseline. The study was supported by the National Eye Institute.

"The CAPT data did not support a large effect for statins in decreasing advanced AMD risk in patients who already had large drusen in both eyes," said lead researcher Maureen G. Maguire, PhD, Department of Ophthalmology, University of Pennsylvania. Drusen are whitish deposits, common in the eyes of people older than 60, which may signal AMD. Statin users were at slightly higher risk than non-users for developing advanced AMD, she said.

Dr. Maguire said several factors may be masking a protective effect for statins, the most important being that most patients who take statins for CVD are also at high risk for AMD. Only a randomized controlled trial could reveal statins' impact on AMD in the wider population, but since so many elderly people take statins it could be difficult to recruit a control group. It is also possible that statins may need to be taken for longer than the CAPT study's timeframe to show a protective effect, she added.

For more information go to www.maculardegenerationassociation.org

Friday, November 27, 2009

Avastin – Wet Macular Degeneration

Learn more about ways to help stop your macular degeneration by clicking on this sentence.

Avastin is the brand name for Bevaciumab a monoclonal antibody or an antibody that is an identical clone of a single parent cell. It was approved in 2004 by the FDA for use in the treatment of some cancers and is used as a first or second line treatment for patients.

As the first clinically available angiogenesis inhibitor the United States it inhibits new cancer cells by blocking the growth of blood vessels in pre-existing tumors. A solid, non-liquid, tumor needs to grow additional blood vessels to be able to reach a certain size.

With an angiostatic agent such as Avastin the growth of new blood vessels is slowed stopping the cancer from growing indefinitely. It is usually given every 14 days intravenously in the arm and can be used with other drugs in combination and with intravenous 5-fluorouracil-based chemotherapy.

Developed by Genentech (NYSE: DNA), a leading biotechnology corporation, it is marketed in the United States under the Genentech name and outside the US under Roche.

When it was originally available in 2004 it was only FDA approved for the treatment of many forms of small cell lung cancer and metastatic colon cancer. A metastatic cancer, in this case colon cancer, is a cancer that spreads from one part or organ to another non-adjacent part or organ.

In 2008 the FDA opened up the doors and allowed for the treatment of breast cancer. There are also clinical trials under way to use Avastin for the treatment of non-metastatic colon cancer, metastatic renal cell carcinoma, metastatic breast cancer, metastatic glioblastoma multiform, metastatic hormone-refractory prostate cancer, metastatic or unresectable locally advanced pancreatic cancer, and metastatic ovarian cancer.

Avastin is also currently being used off-label, the practice of prescribing drugs for a purpose outside the scope of the drug’s approved label, for the treatment of wet macular degeneration by some retinal specialists.

Wet macular degeneration or AMD is a condition that causes loss of vision from the growth of abnormal blood vessel choriocapillaries, through Bruch’s membrane. This eventually leads to blood and protein leaking below the macula, an oval spot near the middle of the retina in the human eye. With AMD rapid, often irreversible vision loss can occur through the leaking, bleeding and scaring of the blood vessels if left untreated.

Dr. Philip J Rosenfeld, MD, PhD of the Bascom Palmer Eye Institute conducted a study that showed positive results for the treatment of AMD with Avastin. According to Dr. Rosenfeld’s study Avastin improved vision in as little as one week for patients treated for AMD.

For AMD treatment Avastin is used in very low amounts by retinal specialists. They usually have a pharmacists transfer the drug from the original vile to a pre-filled needles containing single doses. The specialists will then usually treat the patient in their own office.

As with any drug it is always best to talk to your doctor or pharmacist before starting any treatment.

For more information go to www.maculardegenerationassociation.org

Monday, November 16, 2009

New treatment proves that Macular Degeneration can be cured

Micro Current Stimulation (MCS) which like acupuncture for the eyes. This procedure has proven results that will improved eye site from 20/100 to 20/60 and from 20/25 to 20/20. MD is the destruction of cells in the central part of the retina. A new revolutionary (MSC) treatment will reverse the disease. This treatment will re-generate the cells in the retina as it re-charges the cells and give them new life. This procedure increases the cells production of an energy chemical called ATP which creates new protein. Based on reports from patients this procedure has astonishing results.
For more information go to www.maculardegenerationassociation.org

Monday, November 9, 2009

Treatment for macular degeneration

By Emily Singer
Molecular Sunglasses for Macular Degeneration
Dampening a light-sensing reaction in the eye might slow a common cause of blindness.

Molecules designed to slow the production of toxic byproducts in the eye by making it less sensitive to light are now being tested in patients with macular degeneration, the leading cause of blindness in people age 50 and older. If successful, the compounds would provide a much needed therapy for the disease, which affects more than 15 million people in the United States.
In macular degeneration, cells in the center of the eye, called the macula, deteriorate. A handful of new treatments for the more severe form of the disease, known as wet AMD, have been approved in recent years. But no treatments are yet available for the dry form, which accounts for about 90 percent of cases. Some dry cases ultimately progress to the wet form, which accounts for a large part of AMD-related blindness. “If you can treat dry AMD, you can kill two birds with one stone,” both reducing early symptoms and preventing progression to the wet form, says Paul Sieving, director of the National Eye Institute, in Bethesda, MD.
While scientists are still trying to understand the causes of AMD–age is the biggest risk factor, with genetics and lifestyle factors also playing a role–a growing pool of evidence suggests that the build up of specific compounds in the eye can hasten the cellular damage that underlies the disease. These compounds accumulate in the photoreceptors–cells in the retina that detect light–during normal eye function as the light-sensitive pigments in these cells change conformation in response to photons.
One form of the photopigment, a derivative of vitamin A, is highly reactive and leaks into nearby tissue called the retinal pigment epithelium. “Over time we think these compounds are a burden for the retinal pigment epithelium, which is essential for the healthy function of the photoreceptors,” says Janet Sparrow, director of the Retinal Cell Biology Laboratory at Columbia University, in New York. “In age-related macular degeneration, particularly the dry form, these cells die, and the photoreceptors follow.”
While this reaction is vital for sight, researchers believe that slowing the cycle in the subset of photoreceptors responsible for night vision, known as rods, could slow damage without having a large impact on daytime vision. (Preliminary results suggest it can affect dark-adaptation–when our eyes adjust to low-light conditions.) “During the daytime, the rods are spinning like crazy, wasting vitamin A for no good use,” says Ryo Kubota, an ophthalmologist and founder of Acucela, a Seattle-based startup that is developing treatments for macular degeneration. “It’s like a CCD camera pointed at the sun.”
One compound developed by Acucela that is in clinical trials inhibits the enzyme that converts the photopigment in photoreceptors from one form to another. This process happens only in the eye, allowing the drug to be administered systemically without affecting other tissue, says Kubota. The company has finished initial safety testing in humans and plans to begin a clinical trial assessing the compound’s effectiveness in patients with late-stage dry macular degeneration in a few weeks. Kubota also aims to test the compound in diabetic retinopathy and Stargardt disease, a rare, genetically inherited form of macular degeneration.
A second drug that acts by a slightly different mechanism is being evaluated for macular degeneration by Sirion Therapeutics, a Florida-based pharmaceutical company. The compound is a synthetic vitamin A derivative that is thought to reduce toxin buildup by binding to one of the proteins involved in the reaction. According to preliminary results from tests of the drug in patients with late-stage dry macular degeneration, it can slow the scarring that is characteristic of the disease by 45 percent. However, scientists won’t know if the results are statistically significant until completion of the study next year. Because no treatments have been approved for dry AMD, the U.S. Food and Drug Administration has fast-tracked the drug, speeding the review process.

For more information go to www.maculardegenerationassociation.org

Tuesday, October 27, 2009

AMD Drug And IOP; Getting Good Eyeglasses To Those In Need

A first-time finding of intraocular pressure increases in patients with no personal or family history of glaucoma following anti-VEGF treatment for wet age-related macular degeneration (AMD), and a report on a simple, low-cost method that could revolutionize vision screening and treatment in developing countries, are highlights of today's Scientific Program of the 2009 Joint Meeting of the American Academy of Ophthalmology (AAO) and the Pan-American Association of Ophthalmology (PAAO).

The AAO-PAAO meeting is in session October 24 through 27 at the Moscone Center, San Francisco, CA. As the largest, most comprehensive ophthalmic education conference in the world, it offers United States and international Eye M.D.s more than 2,000 scientifically-based, peer-reviewed presentations including instruction courses, skills labs, "Breakfast with the Experts" roundtables and 900 research papers and posters.

Wet Macular Degeneration Treatment May Increase Intraocular Pressure

Some patients with age-related macular degeneration (AMD) develop elevated pressure within the eye (intraocular pressure, IOP) following treatment with anti-VEGF medications bevacizumab and/or ranibizumab, reports a Yale University School of Medicine study led by Ron A. Adelman, MD, MPH. Both of these anti-VEGFs control the abnormal growth of blood vessels in the eye's retina and are very effective against wet AMD, which can result in vision loss or blindness if untreated. But high IOP is a key factor in glaucoma, also a potentially blinding disease. Of 116 Yale study patients treated for wet AMD with either or both medications from 2006 to 2008, 3.45 percent (four patients) developed a significant and persistent rise in IOP.

"To our knowledge, ours is the first study to document persistent ocular hypertension (OHT) following intravitreal bevacizumab injections in patients with no personal or family history of glaucoma or ocular hypertension (OHT)," Dr. Adelman said. "We found that sustained, high IOP may occur after only one anti-VEGF injection, but more typically after multiple injections. Patients' OHT may continue over several AMD treatments and may require IOP-lowering therapy," he added.

The researchers also reviewed a report by S.F. Bakri and colleagues on persistent OHT after ranibizumab treatment. Of eight OHT patients total in the two studies, four had received a YAG posterior capsulotomy (a procedure related to cataract surgery) prior to wet AMD treatment, which might have predisposed them to OHT, Dr. Adelman said.

New Screening Method Could Mean Clear Vision for Millions

More than 150 million people globally–particularly in developing countries–struggle with poor vision because they cannot access appropriate eyeglasses. Earlier studies indicated that many could not meet the 20/60 vision driver's license standard, a level of impairment that makes daily tasks and economic success difficult. Seeking a low-cost solution, Thomas S. Shane, MD, Bascom Palmer Eye Institute, University of Miami, developed a method that uses a new electronic device called an auto-refractor, a vision chart, and pre-made eyeglasses.

Dr. Shane tested this method in high-poverty Mayan villages in southern Belize. Local health workers recruited people, and everyone over age 12 who came to the clinic within a five-day period was tested. In less than a minute per patient the auto-refractor assessed vision and reported the patient's lens prescription. Of 385 villagers screened 79 needed eyeglasses. Each person received new, pre-made eyeglasses with the appropriate lens strengths; then vision was tested again. On average, vision improved from 20/60 without glasses to 20/25 with glasses.

"This method requires minimal health care worker training and treatment time per patient," Dr. Shane said. "Costs are further minimized because eyeglasses with a range of lens prescriptions to treat the most common refractive errors could be produced and shipped in bulk. Compared to current practices in developing countries, our method may be much more effective, especially where the need is great but resources are limited."

For more information go to www.maculardegenerationassociation.org

Thursday, October 22, 2009

Bionic Eye Opens New World Of Sight For The Blind

Stem cells and electronics can help restore vision to people who’ve been blinded by retinal diseases, scientists reported in Chicago at Neuroscience 2009, the annual meeting of the Society for Neuroscience.

Diseases of the retina cause blindness by damaging the cells that line the back of the eye, where images of the world are normally transformed into nerve impulses that go to the brain.

“There’s very little therapeutic treatment out there tight now for people with diseased retinas,” says Brian Mech, a vice president of Second Sight Medical Products in Sylmar, Calif.

But Second Sight is hoping to change that. The company has developed an experimental bionic eye that has been tried in more than 30 patients with macular degeneration or retinitis pigmentosa.

Building An Artificial Retina

Each patient wears a pair of glasses that incorporates a video camera, Mech says. The video signal from the camera is sent to an implant on the eye itself, which in turns communicates with an array of electrodes attached to the patient’s retina.

And those electrodes do what the old retina can’t anymore: send electrical signals to the brain that allow sight.

Mech says it usually takes patients’ brains a little while to make sense of the new signals.

“They learn to use the device better over time,” he says. “Someone that has had the device for a year will do better than they did at three months.”

The artificial eye uses just 60 electrodes to replace millions of retinal cells. Mech says that means vision is rudimentary.

So people can find doors and follow lines on the floor. But most can’t read, and those who can only make out very large letters.

At the neuroscience meeting, Second Sight presented a study showing that patients could use the artificial eye to tell which direction an object was moving.

Despite the limitations of the artificial eye, Mech says patients who’ve gotten one tend to get emotional when they realize they can see even a little bit.

“There’s a lot of crying, a lot of smiling,” he says. “It’s a sensory input that they haven’t had in a very long time, and so they’re excited.”

Growing New Retina Cells

A team led by Robert Aramant of the University of California, Irvine, offered a different approach to restoring sight.

Since the 1980s, Aramant has been working to fix retinas damaged by diseases including macular degeneration and retinitis pigmentosa.

And for several years now, the team has been treating patients using fetal retinal cells. Their approach is to retrieve an intact sheet of fetal retinal cells and transplant the entire sheet into a damaged eye.

The transplanted cells then mature the same way they would in a developing fetus, creating all the layers of a normal retina, Aramant says.

The team has treated just 10 patients so far, because of funding constraints. But Aramant says seven of those patients got better, including one woman whose vision went from 20-800, which is severely impaired, to 20-200, which is good enough for many daily tasks.

After treatment, Aramant says, the woman was able to play computer games, write emails, and read a large-print version of Reader’s Digest.

Also at the meeting in Chicago, scientists presented studies showing ways to create new light-sensitive molecules in the eye, and to use stem cells to grow specific types of retinal cells.

For more information go to www.maculardegenerationassociation.org

Tuesday, October 13, 2009

MacuCLEAR And Mystic Successfully Complete Phase Ib Clinical Trial For Macular Degeneration

MacuCLEAR, Inc. ("MacuCLEAR") and Mystic Pharmaceuticals, Inc., ("Mystic") announced preliminary successful results of a Phase Ib Clinical Trial for the treatment and prevention of the progression of Age Related Macular Degeneration (AMD). The preliminary results indicated that MacuCLEAR's MC-1101 drug is safe and well tolerated by study participants, and has a biological effect on blood flow in the back of the retina. Mystic's VersiDoser™ ophthalmic delivery system was used by trial participants to self-administer MC-1101 to the front of the eye during the trial. The study included Proof Of Concept ("POC") indicators. A key finding of the study was the successful migration of the drug to the back of the eye.

"We are very pleased with the groundbreaking results of this study," said Philip G. Ralston, Jr., President and CEO of MacuCLEAR. "We have confirmed the safety of MC-1101 in humans, a primary endpoint for the study." Ralston added, "We are excited about the implications of the proof of concept part of this study. Using special laser Doppler flow instrumentation, we showed MC-1101 gets to the back of the eye and significantly modulates the blood flow in the choroid, the tiny blood vessels in the back of the macula portion of the retina. This study provides additional scientific evidence supporting our theory that restoring blood flow in the choroid will have a positive affect on preventing the progression of this terrible disease that is the leading cause of blindness for people over the age of 50 in the world." MacuCLEAR will publish the full results of study later this year.

Mystic Pharmaceuticals' President and CEO, Timothy Sullivan, stated, "We are pleased to have partnered with MacuCLEAR to develop a drug/delivery system combination that has the potential to provide a simpler, safer and ultimately cost effective solution to the millions of people suffering from this disease." Ralston added that, "Mystic's delivery system provided key benefits for both MacuCLEAR and the trial participants. Mystic's novel unit dose approach to packaging each eyedrop individually enabled us to use a preservative free formulation and the control Mystic's technology provides for calibrated precision dose delivery and spray plume definitely enhanced absorption of the drug to the back of the eye." Patients were able to safely and effectively self-administer MC-1101 throughout the trial using the VersiDoser system. "An overwhelming majority of the trial participants expressed a strong positive preference for using the VersiDoser Delivery System over traditional eye drop delivery," Sullivan concluded. Mystic will publish study results of trial participant preferences for its VersiDoser Delivery System later this year.

Ralston and Sullivan presented a summary of the trial results at the Texas Emerging Technology Fund Investment Symposium on October 8, 2009 at the Renaissance Hotel in Richardson, Texas. MacuCLEAR and Mystic presented the status of the progress of their companies at this symposium featuring companies that have received investments from the State of Texas Emerging Technology Fund.

For more information go to www.maculardegenerationassociation.org

Monday, October 5, 2009

NeoVista Presents 24-month Visual Acuity Data Outcomes of Novel Therapy for the Treatment of Neovascular Age-Related Macular Degeneration

NeoVista, Inc. made public today at the Combined Retina Meeting, 24-month data from the company's Phase II study (NVI-111). The study was designed to examine the company's novel epimacular brachytherapy procedure when used in conjunction with Bevacizumab anti-VEGF therapy for the treatment of neovascular age-related macular degeneration (AMD). The long-term data from the study showed that a majority of patients maintained their visual acuity and at least 20% also experienced a marked improvement in vision at month 24. The data also showed that 76 percent of the patients only needed 2 protocol required injections of Avastin® throughout the 24-month period.

"We're excited with the latest data from this Phase II study, said John N. Hendrick, President and CEO of NeoVista. "Safety remains the primary purpose of this study and to date there is no evidence of long-term radiation toxicity at 2 years follow-up, with many patients being followed for as long as 3 years. A large majority of patients in the study maintained their visual acuity over the course of follow-up, while some patients in the trial experienced significant vision gain. We are encouraged by the reduction in the number of injections delivered to patients in this study (mean of 2.4 injections over the 24 month period). This therapy has the potential to decrease treatment burden both for patients and physicians, not to mention the overall financial burden for healthcare systems around the world."

In contrast to other forms of radiation therapy for wet AMD, NeoVista's approach delivers a focused dose of energy directly to the choroidal neovascular lesion without damaging the adjacent healthy retinal vasculature. Utilizing strontium 90, the focused energy is delivered to a target area up to 3 mm in depth and up to 5.4 mm in diameter. Importantly for patients, the systemic exposure to radiation is minimal, as the effective dose to the entire body from NeoVista's epimacular device is less than that from a typical chest x-ray.

The ongoing multicenter feasibility study enrolled 34 trial participants (with a mean age of 72 years) from June 2006 to April 2007 at two centers in Brazil and one in Mexico. These patients, with predominantly classic, minimally classic, or occult (with no classic) choroidal neovascularization (CNV), received a single exposure of epimacular brachytherapy in combination with two intravitreal injections of Avastin, one dose prior to or at the time of radiation delivery and another one month later, depending on which arm of the trial the patient was enrolled in. Additional therapy was delivered based upon the investigator's evaluation of disease activity.

There was an expected increase in the incidence (50%) of cataract formation related to the vitrectomy, the surgical procedure performed when administering epimacular brachytherapy. Comparative data was examined to look at outcomes of patients who entered the study with their natural lens versus those who had already undergone cataract surgery. This analysis showed that 80% of patients who had cataract surgery prior to study entry maintained their visual acuity and 30% gained significant vision at 24 months. When comparing to the cohort of patients that entered the study with their natural lens, 65% percent of patients maintained their visual acuity and 20% percent had significant vision gain, highlighting the fact that cataract formation played a role in long term visual acuity data..

There were a limited number of adverse events in the trial which were related to the vitrectomy procedure (retinal tear, retinal detachment, subretinal hemorrhage, and vitreous hemorrhage), rather than the epimacular brachytherapy. To date, no instances of radiation toxicity have been reported with many patients followed for as long as 3 years.

The data were presented by Pravin U. Dugel, MD, managing partner, Retina Consultants of Arizona, Phoenix, AZ. "The potential of this treatment is enormous", said Dr. Dugel. "I believe that epimacular brachytherapy will be used in combination with the current standard of care to make this treatment more effective by offering a broad spectrum of action. In addition, epimacular brachytherapy may also improve the quality of life for our patients by relieving them from having to receive monthly intraocular injections. The potential impact of epimacular brachytherapy for patients, physicians and the entire healthcare system is prodigious".

NeoVista has recently completed enrollment in the company's first pivotal trial, CABERNET (CNV Secondary to AMD Treated with BEta RadiatioN Epiretinal Therapy). CABERNET is a multicenter, randomized, controlled study that has enrolled 450 subjects at 45 sites worldwide, and is evaluating the safety and efficacy of NeoVista's therapy delivered concomitantly with the FDA-approved anti-VEGF therapy Lucentis® (ranibizumab) versus Lucentis alone.

For more information go to www.maculardegenerationassociation.org

Friday, September 25, 2009

ThromboGenics Completes Patient Enrolment in US Phase III Trial of Microplasmin for the Non-Surgical Treatment of Eye Disease

LEUVEN, Belgium, September 24 /PRNewswire-FirstCall/ --

- Enrolment of 326 Patients Completed Ahead of Schedule

ThromboGenics NV (Euronext Brussels: THR), a biopharmaceutical company focused on the discovery and development of innovative treatments for eye disease, vascular disease and cancer, announces today that it has completed the enrolment of the US Phase III trial evaluating microplasmin for the non-surgical treatment of eye disease. The trial TG-MV-006 has completed enrolment with a total of 326 patients several months ahead of schedule. The second Phase III study with microplasmin, TG-MV-007, which is recruiting patients in the US and Europe is due to complete enrolment in the first half of 2010 as planned. Enrolment completion in this study means that ThromboGenics is a step closer to becoming a profitable, integrated Company focused on cutting edge ophthalmic medicines.

Microplasmin's Phase III program is referred to as the MIVI-TRUST (Microplasmin for IntraVitreous Injection-Traction Release without Surgical Treatment) program. This program involves two clinical trials, which are taking place in the United States (TG-MV-006 trial) and Europe and the United States (TG-MV-007 trial). Both of the MIVI-TRUST trials are multi-center, randomized, placebo controlled, double-masked trials which are evaluating 125microg of microplasmin versus placebo in the intravitreal treatment of patients with focal vitreomacular adhesion.

The initial indication for both of the Phase III microplasmin trials is the non-surgical treatment of focal vitreomacular adhesion. Focal vitreomacular adhesion is a condition in which the vitreous gel, in the center of the eye, has an abnormally strong adhesion to the retina at the back of the eye. Vitreomacular adhesion is thought to play a key role in numerous back of the eye conditions such as macular hole formation, and some forms of macular edema. Vitreomacular adhesion is also associated with a much poorer prognosis in certain major eye conditions, including diabetic retinopathy and Age-related Macular Degeneration (AMD).

The primary endpoint of both trials is the non-surgical resolution of focal vitreomacular adhesion after one month. This anatomical endpoint is being measured and recorded using optical coherence tomography (OCT) which provides images that can clearly show the separation of the vitreous from the retina. OCT is a very sensitive and specific method for detecting the resolution of focal vitreomacular adhesion. ThromboGenics has used both OCT and ultrasound technology in previous studies evaluating microplasmin in eye disease. Based on this experience and discussions with the FDA, OCT was selected as the main assessment technique for the Phase III program as it provides results which have greater clinical relevance. In addition to the primary endpoint, the Phase III trials will evaluate additional measures of efficacy as well as safety, assessed at various time periods over the six month study period.

It is expected that the results from the TG-MV-006 study will be presented by mid 2010.

Dr. Patrik De Haes, CEO of ThromboGenics commented, "We are very pleased to announce that we have completed enrolment of the US pivotal Phase III trial for microplasmin months ahead of schedule. Microplasmin is key to the success of our ophthalmic focused strategy and the speed at which patients have been recruited is very encouraging. Today's announcement brings us a step closer to potentially changing the way a number of important eye conditions are treated, as well as bringing us closer to our key aim of becoming a profitable, integrated business focused on cutting edge ophthalmic medicines. We very much look forward to announcing the results of this trial by the middle of next year and I am confident that ThromboGenics will continue to deliver on the milestones needed to build a strong, successful and profitable Company."

For more information go to www.maculardegenerationassociation.org

Friday, September 18, 2009

Zeaxanthin Supplements Help Prevent Age-Related Macular Degeneration

Author: Lisa Murray

Living longer is what people do now. The number of people suffering from age related disease is on the increase. One of the things people value the most is their sight so what can we do to protect our vision, we can add a supplement called zeaxanthin to our daily diet. Zeaxanthin is a carotenoid found in the central macula of the eye and it helps us to see things straight in front of us such as signs and faces.

A lot of optometrists and ophthalmologists are recommending zeaxanthin supplements for their older patients that are at high risk for age-related macular degeneration. Age-related macular degeneration or AMD is the major cause of blindness in the elderly and simply taking a daily dose of zeaxanthin can help prevent AMD from occurring.

AMD affects 10% of people aged 66-74 years and 30% aged 75-85 years of age. If you have a relative with AMD your chances of developing this disease increase to 50%. Taking a zeaxanthin supplement can change these odds.

Some doctors are recommending zeaxanthin supplements for younger patients as a preventative measure and if doctors are recommending it as a supplement then that lets you see just how important zeaxanthin is to your eyes, your sight and your way of life.

How would it be that, for the sake of one supplement containing 10mg of zeaxanthin you lost your independence, you could no longer see the faces of your family or your favourite books became unreadable. This supplement is more important than ever as we as a society age and demand that we retain our health and our senses while we do so.

Imagine looking at a photograph of a loved one and not being able to see their face. Think about how it would feel to pick up a book or magazine and not be able to read the words right in front of you. Zeaxanthin can help prevent this from happening to you. Imagine your favourite sport, chat show, drama, film or soap opera on the television and not being able to see what was going on in the middle of the screen. Now imagine that you chose a zeaxanthin supplement that suited your needs, took it regularly and made it a part of your health maintenance routine and you won’t have to imagine the loss of your central vision.

Of course zeaxanthin occurs naturally in our eyes and therefore can be found in other places in nature such as fruit and vegetables. Although many of us have improved our diet and take to heart the advice of five portions of fruit and veg each day, this is such an important health issue that it makes sense to ensure that we get enough zeaxanthin into our diet by taking it in supplement form to compliment our healthy eating plans.

As part of what we do we have scoured the supplement market place and found what we believe to be one of the best zeaxanthin supplements currently available. After thoroughly investigating this topic three of our researchers have started taking a zeaxanthin supplement and they are in their thirties. Your sight is something that can be protected from AMD whatever your age, why not start today.

Lisa Murray is an editor of http://www.supersupplementguide.com and is a keen advocate of ensuring your body is properly fueled with the right nutrients in order to give you the healthiest life possible. She does this by taking a carefully balanced multi-vitamin daily. Why not join her today and live life to the fullest for longer.

For more information go to www.maculardegenerationassociation.org

Wednesday, September 9, 2009

New techniques slow progress of age-related vision loss

(CNN) -- When Albert Budacz was young, he prided himself on having good eyesight; he never wore glasses. But as he eased into his late 40s, he couldn't see as well. "I noticed a change in my vision," he explained. "Primarily in church when I would open a Bible, or something like that, I had to position myself under a light to see it."

Concerned that he was beginning to lose his sight, Budacz went to his ophthalmologist, Dr. Sharon Solomon with the Wilmer Eye Institute at Johns Hopkins. He was found to have the beginnings macular degeneration, an eye condition that occurs when the central portion of the retina -- called the macula -- begins to deteriorate.

Until recently, people with age-related macular degeneration, the leading cause of severe vision loss in Americans older than 60, had few treatment options. But now, thanks to new research and advancing technology, there are more vision-saving choices.

Early signs of macular degeneration-related vision loss include shadowy areas or fuzzy distortion in a person's central vision.

"A patient told me recently that he noticed when he was driving that the streetlights were slanted; the poles themselves were slanted," Solomon said. "That's a classic sign of the beginning of this disease."

Although obesity, smoking, high blood pressure and certain drugs can cause it, age is the primary risk factor.

"As people approach their 50s and later, they may have little yellow deposits that develop underneath the retina, and that's called drusen," Solomon explained. "Those deposits are the hallmark of what we call early age-related macular degeneration."

There are two forms of age-related macular degeneration, or AMD: the dry form, known as non-neovascular, and the wet form, called neovascular.

The dry form, which Budacz has, is more common. According to the National Eye Institute, about 85 to 90 percent of patients with advanced macular degeneration have the dry form.

Dry macular degeneration is caused when drusen begin to accumulate in and around the macula. Drusen, those yellowish deposits, are debris from deteriorating tissue.

With dry AMD, there is usually a gradual loss of central vision. Over a period of years, dry AMD can progress to a gradual deterioration of retinal cells, which can result in severe vision loss or lead to the wet version of AMD.

As of now, there is no FDA-approved treatment for dry macular degeneration, although a few drugs and devices are in clinical trials.

However, studies have shown that supplements and a healthy diet can slow the progression of dry macular degeneration. A recent National Eye Institute study found that certain nutrients such as beta carotene (vitamin A) and vitamins C and E may reduce the risk of progression of early-stage AMD by 25 percent.

Solomon says these antioxidants have a positive effect. "They're known as 'preservision,' " she said, noting that they are commonly given to certain patient groups to slow their progression to advanced macular degeneration.

Other research has shown that B6, B12 and folic acid may help prevent age-related macular degeneration. In a study of more than 5,000 women, researchers noted those who took a combination of B6 and B12 vitamins along with a folic acid supplement had a 34 percent lower risk of developing AMD then those taking a placebo.

Although the studies showed strong results, the American Academy of Ophthalmology cautions patients to talk to their eye doctors about which supplements are best for their condition before they start popping vitamins.

In the wet version of macular degeneration, abnormal blood vessels grow beneath the retina and leak blood and fluid. This leakage causes permanent damage to light-sensitive retinal cells, which die off and create blind spots in central vision.

Doctors say it's the body's misguided way of attempting to supply the retina with more nutrients and oxygen. Instead, the attempt creates scarring, leading to severe central vision loss.

Up until recently, there's been very little doctors could do for the wet form of macular degeneration. But over the past decade, there have been a few treatments developed to slow its progression. Cold lasers are now used to freeze the abnormal blood vessels responsible for destroying the macula; they have a 60 percent success rate.

And within the past three years, researchers pinpointed a protein in the eye, called vascular endothelial growth factor, that stimulates the development of blood vessels.

Injectable drugs that inhibit VEGF are now FDA-approved and available; without VEGF, there is little to encourage the growth of blood vessels in the retina.

"They actually have a 90 percent chance of stabilizing vision and a 30 to 40 percent chance of improving vision," Solomon said. "This is the first therapy that we've had that can actually [reverse] vision loss."

Most ophthalmologists prefer an ounce of prevention to a pound of cure. They promote yearly eye exams as the easiest way to keep macular degeneration in check -- and warn against waiting for a crisis to schedule a checkup.

"We typically pick up a patient when, all of a sudden, they've had an acute, abrupt loss of vision or change in the quality of their vision," Solomon said. "And sometimes it's too late."

Albert Budacz was lucky. He caught his macular degeneration in time. He's stopped smoking and takes antioxidants to slow the progression of the disease. And although he may not have the eyesight he had as a young man, he can still see pretty well with or without glasses. And to him, that's all that matters.

For more information go to: www.maculardegenerationassociation.org

Wednesday, September 2, 2009

See Clearly With Nutrients

Vision problems plague many people as they get older, and whether it's an inability to read fine print, dry eyes, floaters, or macular degeneration, these impairments interfere significantly with quality of life. That's why for more than a decade I've recommended lutein, zeaxanthin, zinc, bilberry, and other nutrients that target eye health.

These nutrients consistently provide good results-in fact, in just the past month I've heard from three subscribers who began using them. One woman reported that her macular degeneration, a progressive condition that is the leading cause of blindness in older people, is now under control and holding steady. Another says they help with her vision and dry eyes. And a 93-year-old man told me that now his 40-year-old relatives depend on him to read fine print! Look for vision products that contain 15 mg of lutein, 600 mcg zeaxanthin, 50 mg zinc, and 320 mg bilberry, among other nutrients.

Friday, August 28, 2009

Scientists Morph Human Skin Cells Into Retinal Cells

By Molika Ashford

In a stem-cell breakthrough, scientists have illuminated a new way forward in treating diseases of the eye: turning skin cells into eye cells.
The retina is a lush layered field of tissue lining the back of the eye, a complex mix of specialized cells that serve as a transfer station where light signals are absorbed and sent to the brain to be translated into sight.

Researchers from University of Wisconsin, Madison have now created these unique retina cells from lowly skin cells -- opening the possibility that patients with damaged or diseased retinas might some day be able to grow themselves a cure from their own skin.

First, scientists turned the skin cells into IPS cells (induced pluripotent stem cells), the skin-derived stem cells that have emerged as an alternative to embryonic stem cells. Bathed with a cocktail of chemicals, the IPS cells were then morphed into a variety of retinal cells, including the all-important photoreceptors that translate light signals into electrical signals for our brains to parse as vision.

The scientists report that it is exciting not only to be able to create multiple types of retinal cells, but also that the process appears quite similar to normal retinal development (except in a plastic dish). The group also created retinal cells with embryonic stem cells, but the skin cell method offers an advantage -- patients with genetic diseases of the retina could use their skin to grow a crop of diseased retina cells, which could then be subjected to a variety of test treatments in the lab, hopefully hitting on something that works someday.

The cells might also serve as a treatment themselves, whether grown from IPS cells or embryonic stem cells. Previous studies have improved vision in mice by treating their retinas with stem cells, and this development might help extend that research to humans.

Though in a very early stage, the project is a strong step toward new treatments for an array of debilitating vision disorders.

Tuesday, August 4, 2009

UF reports possible breakthrough on treating macular degeneration

By Diane Chun
Staff writer

Published: Saturday, August 1, 2009 at 5:30 p.m.
Last Modified: Saturday, August 1, 2009 at 5:30 p.m.

A new approach to repairing damaged retinas in mice offers a ray of hope for some two million Americans with an age-related eye condition called macular degeneration.

University of Florida researchers report that they were able to program adult stem cells from mice to transform themselves into vision cells, suggesting a potential treatment for one of the most common causes of vision loss in older people.

In a paper to be published in September's Molecular Therapy, scientists describe how they used a virus carrying a gene that gently pushed cultured adult stem cells toward a fate as retinal cells. When the cultured cells were reintroduced into the mice, they were completely transformed into the desired type of vision cells.

"To our knowledge, this is the first reported use of targeted gene manipulation to specifically program an adult stem cell to become a new cell type," said Dr. Maria Grant, professor of pharmacology and therapeutics in the UF College of Medicine.

Ultimately, Grant said, the findings suggest that the same thing could be done with drugs.

"You would not give the drugs to the patient," she explained, "you would give the drugs to their cells. Take the cells out, activate certain chemical pathways, then put the cells back into the patient."

The researchers were able to use chemical compounds that mirrored environmental conditions in the body to point the stem cells toward their ultimate identities as vision cells.

In essence, they were successful in tricking the stem cell into thinking it is a retinal cell and behaving accordingly.

"This implies a whole new field of stem cell research that uses drug manipulation rather than genetic manipulation to send these immature cells along a new pathway," said Grant.

She collaborated in the work with Edward Scott, director of the program in stem cell biology and regenerative medicine at UF's McKnight Brain Institute.

"This work applies to 85 percent of patients who have age-related macular degeneration," Grant said. "There are no therapies for this devastating disease."

for more information contact www.maculardegenerationassociation.org

Sunday, July 12, 2009

Study Published In PNAS Reveals Side Effects Of Experimental "Gene-Silencing" Treatment

The side effects of an experimental "gene-silencing" treatment that is currently being investigated for a variety of diseases are even more wide-ranging than previously discovered, according to a study by a University of Kentucky researcher.

Following up on groundbreaking research published last year in the journal Nature, Dr. Jayakrishna Ambati, a UK ophthalmologist , and his colleagues found that the new drug modality, siRNA (21-nucleotide small-interfering RNA), is toxic not only to blood endothelial cells, which line blood vessels, but also to the cells lining the lymphatic channels.

These findings reinforce the note of caution sounded by Ambati's previous Nature study, which has been cited nearly 50 times and highlighted in special reviews in premier journals such as Cell and in Nature, which termed it "stunning." But these side effects could themselves find useful application, for example, in cornea transplantation, where growth of new blood and lymph vessels is believed to be a major cause of graft failure.

The new findings are published in this week's online issue of Proceedings of the National Academy of Sciences, the official journal of the U.S. National Academy of Sciences.

In the earlier study, the Ambati laboratory discovered previously unrecognized immune side effects of siRNA, which is currently in FDA trials for numerous diseases including age-related macular degeneration and life-threatening viral infections.

Specifically, they showed that in two different established animal models of new blood vessel growth, siRNA killed these cells by activating an immune receptor called toll-like receptor 3 (TLR3). This was a critical finding, as immune and blood vessel toxicities were not believed to occur with this pharmacologic technique. As a result, siRNA is now recognized as a new class of anti-vascular drugs that could potentially be used to treat some of the 10 percent of the world's population suffering from neovascular diseases. However, this first study did not address other forms of specialized endothelial cells that exist in the human body, including those that line the lymphatic system, a critical component of immune responses. The new study found that siRNAs block not only blood vessels but also lymphatic vessels. In the cornea, the clear part of the eye, injury often leads to the formation of both blood and lymphatic vessels. In fact, the formation of lymphatic vessels after corneal transplantation is purported to be a major mechanism through which transplant rejection occurs. Ambati's lab found that corneal injections of siRNA suppressed both blood and lymphatic vessel growth via endothelial cell toxicity.

Won Gil Cho, post-doctoral fellow, Dr. Romulo Albuquerque, and Dr. Mark Kleinman, researchers in the Ambati laboratory, also showed that siRNA directly activates TLR3, the first time this has been demonstrated in the literature. Addditionally, they showed, using time-lapse studies, that siRNA does not enter cells without a cell-permeating moiety such as cholesterol. This is important, because siRNA must enter cells in order to function as intended by specifically degrading intracellular messenger RNA bound for protein-forming machinery. Furthermore, this finding strengthens their finding that TLR3 positioned on the cell surface is responsible for mediating the toxic side-effects of siRNA. In concert with Sandro De Falco and Arturo Brunetti, researchers in Naples, Italy, they also found that siRNAs generically block blood and lymphatic vessel growth in muscle tissue as well. These findings illustrate this side effect of siRNA can occur in many parts of the body.

Ambati's lab also reported last year in the New England Journal of Medicine that siRNA is deleterious to other cell types, such as the retinal pigmented epithelium, which is involved in age-related macular degeneration.

"This may be a broadly imprinted response in the mammalian immune system that is activated by siRNA," Ambati said. "In terms of benefit, siRNA may be utilized in the treatment of diseases of the lymphatic system, including lymphangiomas for which there is currently no effective targeted pharmacologic intervention."

Ambati is a Doris Duke Charitable Foundation Distinguished Clinical Scientist and a Burroughs Wellcome Fund Clinical Scientist in Translational Research. His laboratory is also supported by the National Eye Institute of the NIH, Research to Prevent Blindness, and American Health Assistance Foundation.

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).

Saturday, May 30, 2009

First Bionic Eye to Undergo Clinical Tests by 2011

The first clinical tests of a bionic eye are likely within two years and commercialization within five, according to researchers.

A bionic eye is a form of neural prosthesis intended to partially restore lost vision or amplify existing vision.

There is a lot of promising research being done right now. We are living in a very exciting time.

However, we can't put our plans and dreams on hold until this research delivers a cure.

I will never forget the day that I discovered a Telesensory video magnifier in a university library. It was 1977. I was just about to drop out of college before I made this discovery.

That video magnifier made it possible for me to complete college and live my dream as a public school teacher for 21 years!

Today I am very proud to own Amazing Video Magnifiers where I distribute only Telesensory video magnifiers.

They are, in my opinion, the most reliable and cost efficient.

I encourage you to visit the site and read about the various outstanding units.

Sunday, May 10, 2009

New Medical Study Establishes First-Ever Long-Term Benefits for Macular Degeneration Sufferers Using Macular Health Vitamin Supplement

New Medical Study Establishes First-Ever Long-Term Benefits for Macular Degeneration Sufferers Using Macular Health Vitamin Supplement

Eye disease product has the potential to preserve vision for millions

BIRMINGHAM, Ala., April 28 /PRNewswire/ -- As many as 17.8 million people will suffer from age-related macular degeneration (AMD) by 2050 and 1.57 million will be blind from the disease, according to the U.S. Centers for Disease Control and Prevention. However, a new medical study by a group of retina specialists at the Callahan Eye Foundation Hospital at the University of Alabama Birmingham (UAB) indicates that with the use of the Macular Health vitamin supplement there is a way to reduce these numbers and potentially preserve the vision of millions.

The second phase of the Multifocal Electroretinogram (MERG) study recently revealed that patients suffering from AMD experienced long-term benefits from taking Macular Health, a special combination of supplemental vitamins, minerals and carotenoids. Phase I of the MERG study, completed in 2005, confirmed an average of 16 percent improvement in vision after taking Macular Health for only 12 weeks. Phase II measured the vision function of the same patients two years later and found an average improvement in vision of 17 percent.

"The outcome of this study is extremely encouraging for sufferers of age-related macular degeneration," says John O. Mason, III, MD, researcher and retinal specialist at the Callahan Eye Foundation Hospital. "These new findings prove that Macular Health can slow vision loss and actually improve vision function over time."

MERG testing was used to gauge the vision of AMD patients before and after using the Macular Health supplement. The test results of patients taking Macular Health were compared to results of a control group that did not take the supplement. Phase II of the study was accepted by the Association for Research and Vision in Ophthalmology (ARVO) for poster presentation. Mason and a team of retina specialists will continue to monitor study participants to evaluate improvement in eye health and vision with the use of Macular Health.

Jeffery McAnnally, President of Macular Health, LLC, says, "On behalf of the Macular Health Company, I am pleased to share this additional proof of Macular Health's effectiveness. Not only is Macular Health the most affordable product of its kind on the market today, it is the easiest to take."

An estimated 9 million people currently suffer from AMD, and one-third of adults over 70 are afflicted with this incurable disease. AMD is the leading cause of blindness in Americans 50 years of age and older. AMD is a breakdown of the macula of the eye that typically occurs during the aging process. Damage of the macula increases the difficulty of seeing fine details and even faces clearly.

To learn more about age-related macular degeneration or the Macular Health vitamin supplement, visit www.macularhealth.com. To speak with John O. Mason, III, MD, please contact Julie Ward at 205.503.5955 or julie@styleadvertising.com.
Website: http://www.macularhealth.com/

Sunday, May 3, 2009

Possible Cure on Horizon

It's a sight for sore eyes.

Stem cell therapy to cure blindness is being developed by British scientists, and surgeons believe it could become a simple procedure that will be available in six or seven years' time, the London Times reported.

The process involves replacing a layer of dying cells with fresh ones created from embryonic stem cells.

It targets age-related macular degeneration (AMD), one of the most common causes of blindness, which involves the loss of eye cells.

"This is a huge step forward for patients," Tom Bremridge, chief executive of the Macular Disease Society, told the Times. "We are extremely pleased that the big guns have become involved, because, once this treatment is validated, it will be made available to a huge volume of patients."

Embryonic stem cells have the ability to develop into all types of body tissue.

Their use is controversial, however, because it involves the destruction of human embryos.

Lab tests done by the British team have shown that stem cells can prevent blindness in rats, and similar elements work on pigs.

A clinical trial is expected within two years.

It will most likely be the second in the world to use embryonic stem cells on humans. The first, spinal cord injury sufferers, will start later this year in the United States.

Sunday, April 26, 2009

Sirion gets FDA Fast Track designation for sight-preserving drug

Sirion gets FDA Fast Track designation for sight-preserving drug
Tampa Bay Business Journal

Sirion Therapeutics Inc. announced positive results from a clinical trial evaluating a treatment for certain persons with macular degeneration.

The Phase II trial evaluated fenretinide as a treatment for geographic atrophy associated with age-related macular degeneration.

Sirion describes fenretinide as an oral vitamin A binding protein antagonist. Geographic atrophy is the most advanced form of dry age-related macular degeneration.

An analysis of the Phase II data showed slower growth of lesions in patients treated with oral fenretinide than in patients who received a placebo, a release from Sirion said.

Sirion will continue the Phase II study and will meet with scientific advisers and the Food and Drug Administration to design a Phase III study, the release said.

The effort by Sirion to develop fenretinide as a treatment got an additional boost when the FDA granted it Fast Track designation, the release said. Fast Track programs of the FDA are designated to facilitate the development of drugs that are intended to treat serious or life threatening conditions and that demonstrate the potential to address an unmet medical need for such a condition.

Sirion is a privately held biopharmaceutical company based in Tampa focused on discovery, development and commercialization of products to protect and preserve eyesight.

Sunday, April 19, 2009

New Drug May Help Treat, Reverse Advanced Macular Degeneration
Apr 13, 2009
Reporter: CBS News
Email Address: news@kbtx.com

As the baby boomers age and live longer, a severe sight problem called Macular Degeneration is becoming more common.
But, there are new treatments to help the condition that can lead to blindness.
Sylvia Moore was diagnosed with macular degeneration three years ago.
"If I look straight ahead at somebody's face, I don't see them at all, you'd see a blank spot, a black spot," says Moore of the disease.
Macular Degeneration is most common in seniors.
It happens when blood vessels in the back of the eye start leaking and is the leading cause of blindness in people over 65.
The good news is doctors now have more weapons than ever to fight the condition, and in some cases even reverse it.
When it's caught early, vitamin therapy can slow down the progression of macular degeneration, and in some cases laser surgery can halt vision loss.
But the latest treatment is a drug that's injected directly into the eye.
The medication targets the abnormal blood vessels leading to its shutdown and hopefully to the improvement in vision.
Moore has been getting the injections for three months and is already seeing a difference.
"Its scary when you see a needle coming at you but it doesn't hurt.... I'd rather have that than blindness," Moore says.
A new study predicts some 9 million americans will be diagnosed with macular degeneration next year.
That number is expected to double in the next 40 years.

Saturday, April 11, 2009

Eye 'compensates for blind spot'

Eye 'compensates for blind spot'
Eye Peripheral vision is retained

Partially sighted and registered blind people can be taught to read and see faces again using the undamaged parts of their eyes, say experts.

When only the central vision is lost, as with the leading cause of blindness, age-related macular degeneration, peripheral vision remains intact.

And patients can be taught to exploit this, the Macular Disease Society says.

It has developed a training scheme and is calling for professionals to adopt the system across the UK.

The macula is a small area of the retina at the back of the eye made up of specialist cells which process central vision as well as the fine detail of what we see.

Our scheme has transformed lives - helping people to relearn basic skills they thought to have lost for good
Tom Bremridge
Macular Disease Society

People with macular degeneration rarely go totally blind but even those with a relatively mild version of the disease cannot drive and have difficulty reading, recognising faces and watching television.

But studies show people can be taught to use their peripheral vision to fill in the gaps, using "eccentric viewing" and "steady eye techniques".

When someone with central vision loss looks directly at an object it may disappear, go faint, blur or distort. But when they look above, below or to one side of it, they see it more clearly.

Blind spots

Eccentric viewing helps people find exactly where to focus their gaze to make their vision better.

Once this position is identified, they can be taught how to read again using the steady eye technique.

Instead of moving the eyes from left to right to read a sentence, the person should keep their eyes completely still and move the text to the left so that each word in turn moves into the area of best vision.

All UK patients with central vision loss should have the opportunity to try eccentric viewing
Mr Winfried Amoaku
Royal College of Ophthalmologists

Macular Disease Society chief executive Tom Bremridge said: "Eccentric viewing works by making the most of vision that remains.

"Our scheme has transformed lives - helping people to relearn basic skills they thought to have lost for good.

"We have 86 volunteer trainers, all with central vision loss themselves, who have trained more than 310 people in their own communities, and our waiting list of nearly 1,200 people grows every day.

"We are keen that other service providers - social services, private practitioners and primary care trusts - now take up the baton."

Mr Winfried Amoaku, of the Royal College of Ophthalmologists, said eccentric viewing could help some patients with central vision loss "cope with everyday tasks such as identifying coins while out shopping, watching television and reading".

"The trouble is, we don't know who will benefit until they have tried the training.

"All UK patients with central vision loss should have the opportunity to try eccentric viewing techniques to see if they can benefit," he said.

Marek Karas, of the Royal National Institute of Blind People, also supported the research advances.

"Although there is still ongoing discussion among experts over the best form of training for this type of therapy, we welcome with interest these latest developments."

Between 25 and 30 million people worldwide have macular degeneration. But as the population ages, this figure will rise.

It is estimated that the number of people affected will triple by 2025.

Sunday, April 5, 2009

FDA Approval Recommended for Implantable Macular Degeneration Device

FDA Approval Recommended for Implantable Macular Degeneration Device
By Emily P. Walker, Washington Correspondent, MedPage Today
Published: March 30, 2009

GAITHERSBURG, Md., March 30 -- An FDA advisory panel agreed that the agency should approve a miniature implantable telescope to improve central vision in elderly people with end-stage age-related macular degeneration.

The Ophthalmic Devices Panel voted unanimously Friday to recommend approval for the Implantable Miniature Telescope, made by Vision Care Ophthalmic Technologies, for use in patients who are 65 or older.

The thumbs-up came despite the device's association with loss of corneal cells over time.

Many elderly people would likely choose the telescope -- which could help maintain their ability to carry out daily tasks such as recognizing faces and reading books -- even if it meant developing corneal edema four or five years down the road, the panel decided.

Four years after the implant, about 15% of patients will have a significant depletion in endothelial cells, which can lead to corneal edema, according to an estimate by the panel's biostatistician, Karen Bandeen-Roche, Ph.D., of Johns Hopkins University in Baltimore.

The telescope works by directing light from the lens onto still-functioning portions of the macula to maintain central sight. It increases vision up to about three meters, helping patients perform close-up tasks, though doing nothing for their ability to drive.

The device would be implanted in one eye, after patients wear an external version for a few days to get a feel for it. Because it only improves central vision, implant recipients would rely on the opposite eye for peripheral sight.

The outcome of the Friday meeting was a major victory for the Vision Care, especially because the FDA turned down its original application in 2006 because of safety concerns.

New, longer-term data convinced the panel that the telescope can deliver improved vision for certain patients and that the associated cell loss is an acceptable risk.

Vision Care applied for a much narrower indication this time around. So narrow, in fact, that only about one-quarter of the participants included in the company's original trial would meet the new criteria, according to Henry Hudson, M.D., an vitreoretinal specialist in Tucson, Ariz., and lead investigator of the main clinical study submitted to the FDA.

The device was originally intended for patients 55 and older, but the sponsors bumped the age requirement up to 65. The new application also excludes patients with corneal guttata, and those who have an anterior chamber depth of less than 3 mm. Patients must also have retinal cell counts that are normal for their age group before receiving the implant.

The application calls for the device to be implanted by cornea specialists who are trained by Vision Care.

The panel's approval was based largely on a trial involving 206 patients with incurable central vision disorders and who were over 55 and had a need for cataract surgery.

The primary endpoint for efficacy was improvement of two lines or greater in either near or distance vision, which was achieved in 86% of patients at follow-up.

In a four-year follow-up that the company completed at the request of the FDA, 68% of the patients achieved a two-line or greater gain in either long distance or near vision four years after the surgery.

The panel heard from three octogenarians who said that if it weren't for their implantable telescopes, they would not be able to read books, make crafts, recognize their grandchildren, or carry out daily chores.

The committee suggested that the original trial cohort -- of which 130 are alive and still have the implant -- be followed for additional five years to monitor for complications such as rates of corneal transplant, retinal detachments and corneal edema.

The committee, chaired by Jayne Weiss, M.D., an ophthalmologist from the Kresge Eye Institute in Detroit, also said patients should be informed of the risk of cell loss and the possible benefits of improved central vision associated with the device.

The lead researcher agreed.

"The key consideration is proper patient expectation to get the maximum effect of this technology," Dr. Hudson said.

Monday, March 30, 2009

Positive Results from Neurotech's NT-501 Phase 2 Dry AMD

Positive Results from Neurotech's NT-501 Phase 2 Dry AMD (Geographic Atrophy) Study Demonstrate Proof of Concept


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LINCOLN, R.I.--(BUSINESS WIRE)--Mar 26, 2009 - Neurotech Pharmaceuticals, Inc., today announced that the Company's lead product candidate, NT-501, substantially slowed the loss of vision in a Phase 2 clinical trial in subjects with dry age-related macular degeneration (AMD) involving geographic atrophy (GA). GA is a condition that destroys sharp central vision, often resulting in serious vision loss to one or both eyes. There are currently no approved treatments for dry AMD. In the study, the high dose of NT-501 stabilized best corrected visual acuity (BCVA) at 12-months, with 96.3% (p=0.078) of treated-patients losing fewer than three lines of vision, or 15 letters, versus 75% of the patients in the sham-treatment group.

NT-501 is an intraocular implant that consists of human cells that have been genetically modified to secrete ciliary neurotrophic factor (CNTF). CNTF is delivered directly to the back of the eye in a controlled, continuous basis by means of the Company's proprietary Encapsulated Cell Technology (ECT) platform, thereby bypassing the blood-retinal barrier and overcoming a major obstacle in the treatment of retinal disease.

The Phase 2 study is a multi-centered, randomized, double-masked, sham-controlled study of 51 subjects with GA. Patients received either a high or low dose NT-501 implant or a sham treatment in one eye only and were assessed for changes in BCVA. BCVA was measured by an Electronic Visual Acuity Tester (EVA) using the Early Treatment Diabetic Retinopathy Study (ETDRS) protocol. Patients were also evaluated for an increase in BCVA. However, no increase was observed, likely due to existing photoreceptor damage. There were no NT-501 associated serious adverse events reported and both NT-501 and the surgical procedure were well-tolerated.

“The favorable functional visual acuity results for patients at this advanced stage of dry AMD are particularly promising due to the significant prevalence of the condition, its serious impact on quality of life and the current unmet medical need for effective therapy," stated Dr. George A. Williams, a study investigator and Professor and Chair of the Department of Ophthalmology at William Beaumont Hospital and the Oakland University William Beaumont School of Medicine in Royal Oak, MI.

The strong trend in visual acuity stabilization at 12 months was preceded by a dose-dependent, statistically significant (p<0.001 and p=0.013 for high and low dose, respectively) increase in retinal thickness as measured by optical coherence tomography (OCT) that was observed as early as 4 months post-implantation. The observed structural change is consistent with preclinical studies of NT-501 in which CNTF was shown to increase the thickness of the retina and the outer nuclear layer of photoreceptors responsible for vision. This increase in retinal thickness may be responsible for photoreceptor rescue and protection as observed in numerous animal models of retinal degeneration.

“Based on the increase in retinal thickness observed in this study it appears that CNTF may be exhibiting a biological effect on retinal photoreceptors as has been observed previously in animal studies,” said Dr. Paul Sieving, Director of the National Eye Institute and Principal Investigator of Neurotech's Phase 1 study of NT-501 in retinitis pigmentosa.

“We believe the anatomical changes observed in patients treated with NT-501 have led to the emergence of a clinically meaningful visual acuity benefit for patients with geographic atrophy,” commented Ted Danse, President and Chief Executive Officer of Neurotech. “NT-501 may provide a much needed treatment option for these patients and we intend to discuss these data and a pivotal trial design with the FDA.”

“We are very pleased that the outcome of this trial has shown such promise for patients with dry AMD involving geographic atrophy and are proud of our long-term support for this unique, breakthrough technology,” stated Stephen Rose, PhD, Chief Research Officer, Foundation Fighting Blindness.

Five devices from this trial have been explanted 12 months following implantation and all have been found to have uniformly healthy, viable cells that continue to produce therapeutic levels of CNTF. This is consistent with data from multiple trials of NT-501 in which, to date, 23 devices have been explanted between 12 and 18 months following implantation and all devices have contained healthy, viable CNTF-producing cells.

“We also believe the positive results of this study and long-term cell viability validate our ECT platform and support a breakthrough opportunity to advance long-term, well-tolerated treatments for patients facing chronic sight-stealing retinal diseases. As such, we are developing our second product utilizing the ECT platform to address a well-validated target, anti-VEGF therapy for wet AMD, that has the potential to provide a one-time administration for a 12 to 18 month period versus the current wet AMD treatment regimen that requires monthly injections with routine patient monitoring,” concluded Danse.

Data from the Phase 2 dry AMD/GA trial will be presented at the Retinal Physician Symposium on March 27, 2009 in the Bahamas, at IBC's 5th International Ocular Angiogenesis & Retinal Degeneration conference on March 31, 2009 in Las Vegas, at the Advanced Vitreoretinal Techniques and Technologies meeting on April 24, 2009 in Las Vegas and at the Association for Research in Vision and Ophthalmology (ARVO) meeting on May 6, 2009 in Ft. Lauderdale.

About Dry AMD/Geographic Atrophy

Age-related macular degeneration (AMD) is a chronic progressive disease of the macula that results in the loss of central vision. It is the leading cause of blindness in elderly people in the developed world. There are two forms of AMD•dry and wet. Dry AMD is the most common form of AMD representing approximately 90% of all AMD cases. In its advanced stages dry AMD can lead to the degeneration of photoreceptors and retinal pigment epithelial cells, a chronic condition called geographic atrophy (GA). There are currently no approved GA therapies for the nearly 1 million individuals affected in the United States.

About NT-501

Neurotech's lead product, NT-501, consists of encapsulated human cells genetically modified to secrete ciliary neurotrophic factor (CNTF). CNTF is a growth factor capable of rescuing dying photoreceptors and protecting them from degeneration. NT-501 is designed to continually deliver a therapeutic dose of CNTF into the back of the eye.

About Encapsulated Cell Technology

Neurotech's core technology platform is Encapsulated Cell Technology (ECT), a unique technology that allows for the long-term, sustained delivery of therapeutic factors to the back of the eye. ECT implants consist of cells that have been genetically modified to produce a specific therapeutic protein and are encapsulated in a semi-permeable hollow fiber membrane. The diffusive characteristics of the hollow fiber membrane are designed to promote long-term cell survival by allowing the influx of oxygen and nutrients while simultaneously preventing direct contact of the encapsulated cells with the cellular and molecular elements of the immune system. The cells continuously produce the therapeutic protein which diffuses out of the implant at the target site. ECT thereby enables the controlled, continuous delivery of therapeutic factors directly to the retina, bypassing the blood-retina barrier.

About Neurotech Pharmaceuticals, Inc.

Neurotech is developing sight-saving therapeutics for the treatment of chronic retinal diseases. The Company's lead product candidate, NT-501, is currently in late-stage clinical development for advanced dry age-related macular degeneration (dry AMD) and retinitis pigmentosa (RP). The Company's portfolio of product candidates also includes treatments for wet AMD. All of Neurotech's development programs are based on the Company's proprietary Encapsulated Cell Technology (ECT). ECT uniquely enables the controlled, continuous delivery of biologics directly to the back of the eye, thereby overcoming a major obstacle in the treatment of retinal disease. To learn more, please visit our web site at www.neurotechusa.com.

Saturday, March 21, 2009

Macular degeneration may have same biomarker as kidney function

Macular degeneration may have same biomarker as kidney function
Publish date: Mar 5, 2009
Source:Optamology Times

Madison, WI—Cystatin C, a biomarker of kidney function, also may be associated with the incidence of age-related macular degeneration (AMD), said researchers.

Adjusted analyses found that serum levels of the protein were associated with the incidence of both early and exudative AMD, according to Ronald Klein, MD, MPH, and colleagues.

There was an association between chronic kidney disease and macular degeneration, but the association between cystatin C and the degenerative eye disease was intensified in patients without chronic kidney disease.

"This suggests that this relationship might not be due to kidney-related processes," the researchers said.

Studies on the relationship of kidney disease and AMD have been few and inconsistent, so researchers conducted a prospective cohort study of 4,926 patients aged 43 to 86 years, in Beaver Dam, WI.

Saturday, March 14, 2009

Pill Shows Promise for Treatment of Macular Degeneration

By JEAN ENERSEN / KING 5 News

Beatrice Dean has had the dry form of macular degeneration for 20 years.

"You get to the point where you don't read any longer, you don't write, you just don't see things straight on,” she said.

A National Institute of Health study found that certain eye vitamins can help, to a point. Dr Richard Bensinger of Swedish Medical Center says this was the first breakthrough.

"It showed a very significant slowing of the condition, not a cure, or stoppage,” he said.

Now the Acucela biotech firm in Bothell is working on a pill that may finally stop the disease altogether.

Founder Ryo Kubota says the goal is to prevent dry form from progressing into the more severe wet form, which can cause blindness overnight.

"Primarily it will be preventative and slow down the disease, but in animal test studies that we've done, we've show in can reduce the already accumulated toxic byproducts,” said Dr. Kubota.

In theory, the drug works by blocking the damage before it starts.

Who will get macular degeneration?

"There really is no risk factor that's known except for everybody's favorite, smoking,” said Dr. Kubota.

Dr. Kobota hopes this research will make all the difference since macular degeneration cases are expected to rise as baby boomers get older.

“We're hoping this drug to be on the market in five to 10 years,” he said.

Human trials are just beginning. We'll keep you up to date on the research and when the study will begin recruiting locally.

Saturday, March 7, 2009

Brain Adapts to Age-Related Eye Disease

Brain Adapts to Age-Related Eye Disease
Neurons seek input from undamaged areas to compensate, study finds

Posted March 3, 2009

TUESDAY, March 3 (HealthDay News) -- When macular degeneration causes one to start losing his or her sight, the affected neurons simply start seeking visual input from other, non-affected parts of the eye, Massachusetts Institute of Technology researchers report.

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"This study shows us one way that the brain changes when its inputs change. Neurons seem to want to receive input: When their usual input disappears, they start responding to the next best thing," senior author Nancy Kanwisher, of MIT's McGovern Institute for Brain Research, said in an university news release.

The researchers found when the cells in the fovea, the part of the retina responsible for the central field of vision, were damaged by macular degeneration (MD) -- the neuron attached to them begin responding to stimuli in an undamaged section -- a type of internal reorganization of the eye's visual map as opposed to the cortex's work being shifting to other neurons.

"Our study shows that the changes we see in neural response in people with MD are probably driven by the lack of input to a population of neurons, not by a change in visual information-processing strategy," Kanwisher said.

The findings are published in the March 4 issue of the Journal of Neuroscience.

Macular degeneration, the most common form of adult blindness, affects almost 2 million people in the United States. Patients often compensate for lack of central vision by rolling their eyes upward so they can utilize the preferred retinal locus (PRL), an undamaged area under and adjacent to the affected part of the retina.

"Macular degeneration is a great opportunity to learn more about plasticity in the adult cortex," Kanwisher said.

Wednesday, February 25, 2009

Should everyone with AMD be taking high-dose vitamins?

Only those patients with intermediate to advanced forms of AMD should be taking the high-dose multivitamin formula. Ask your doctor if you should be taking this vitamin supplement.


Is it safe to take high doses of vitamin E?

AREDS researchers say it is unclear if the possible increased risk associated with very high doses - 500IU to 2000IU - of vitamin E applies to people taking 400IU. An increased risk of mortality was not found among those taking about 400IU of vitamin E.

The National Institutes of Health Office of Dietary Supplements has a fact sheet on vitamin E that summarizes the research on vitamin E and different chronic diseases.

Tuesday, February 17, 2009

Will vitamins make my vision better?

Will vitamins make my vision better?

Vitamin therapy for AMD will help slow the progression of AMD. Vitamins are not a cure for AMD and will not give back any vision that has already been lost.

Should everyone with AMD be taking high-dose vitamins?

Only those patients with intermediate to advanced forms of AMD should be taking the high-dose multivitamin formula. Ask your doctor if you should be taking this vitamin supplement.

Thursday, February 12, 2009

Vitamins and AMD

Are vitamins helpful for AMD?

The Age-Related Eye Disease Study (AREDS) showed that taking high-dose anti-oxidant vitamins and zinc significantly slowed the rate of progression of vision loss in patients who had more advanced forms of AMD.

AREDS II is an ongoing study to understand the role of certain other vitamins. More information

What vitamins should I take?

The following vitamin combination was proven effective in the AREDS study:

* Vitamin C, 500 mg
* Vitamin E, 400 IU
* Beta-Carotene, 15 mg
* Zinc, as zinc oxide, 80 mg
* Copper, as cupric oxide, 2 mg

Thursday, February 5, 2009

Vision Loss from Macular Degeneration

By Jacob Teitelbaum, MD on January 30, 2009 in Complementary Medicine

Does the center of your visual field seemed blurred?

Age-Related Macular Degeneration (ARMD) is the most common cause of age related vision loss (besides needing reading glasses). Fortunately, natural treatments are very helpful for both prevention and treatment.

BACKGROUND

The macula is in the central part of the retina that is used for more detailed vision, so it tends to affect the center of our visual field. As it has the largest concentration of cells, it also needs more oxygen then the rest of the retina. ARMD is a degenerative condition of the macula. It is the most common cause of vision loss in the United States in those 50 or older, and increases with age. ARMD is caused by hardening of the arteries that nourish the retina. Fortunately, macular degeneration does not cause total blindness since it does not affect the peripheral vision.

There are 2 types of ARMD:

Wet ARMD

Around 10% of cases are called "Wet" ARMD, as new, but fragile, blood vessels try to regrow in to support the macula. These fragile new vessels sometimes leak (hence the name "Wet") causing rapid vision loss in the center of 1 eye.

Dry ARMD

The other 90% of cases are called "Dry" ARMD, and these have a very gradual progression.

PREVENTION and TREATMENT

A number of studies have shown that good nutrition can slow or prevent the development of macular degeneration. For example, it has been proven that people with diets high in antioxidant containing fruits and vegetables (especially leafy green vegetables and colorful berries) have a lower incidence of macular degeneration. This is associated with high levels of the nutrient flavonoids, as well as lutein and zeaxanthin (both found in egg yolks), and lycopene (in tomatoes). In fact, those with high levels of these nutrients had only half the risk of ARMD. Fish oils and nuts were also very protective. Red wine is protective, but beer can worsen ARMD.

Research suggests that a mix of nutrients is more effective than individual ones for ARMD. I recommend a product called "Ocudyne II" capsules by Nutricology (easily found in many online shops) along with:

* Vitamin C 1,000 mg 2-3x day
* Vitamin E (must be natural and mixed tocopherols) 600 units/day
* Selenium 200 mcg a day
* Ginkgo Biloba (standardized to 24%) 40-80 mg 3x day
* Bilberry extract (25% extract) 40-80 mg 3x day
* Zinc 25-50 mg a day
* Eat fish (especially tuna or salmon at least 2x week) ot take fish oil

Other helpful tips include:

* Protect your eyes with sunglasses that have UV protection. Ultraviolet rays are believed to cause damage to the pigment cells in the retina.
* Quit smoking. Smoking worsens circulation to the retinal blood vessels.

To make reading easier:

* Use a halogen light. These have less glare than standard light bulbs.
* Shine the light directly on your reading material. This improves the contrast and makes the print easier to see.
* Use a hand-held magnifier. A cheap drugstore magnifier can increase the print size dramatically.

For wet ARMD, your eye doctor may recommend laser treatments, which can be added to the treatments above.

Wednesday, January 28, 2009

Researchers Hope to Mime 1000 Neurons With High-Res Artificial Retina

By Sally Adee

19 December 2008—Researchers from three major California universities are working on an artificial retina that could give limited sight to people with degenerative diseases of the retina, such as macular degeneration. Such a prosthesis is a more realistic future treatment than stem-cell therapy, gene therapy, or eye transplants, its developers say. The Californian researchers have been treating people using a 60-pixel retina in a clinical trial for two years. But they are now gunning for a system with a resolution of 1000 pixels, they reported Tuesday at the IEEE International Electron Devices Meeting (IEDM), in San Francisco. And in contrast with systems in trials today, the researchers hope to develop a system that would be completely sealed into the eye, without any external components. 


James Weiland, an associate professor of ophthalmology at the University of Southern California’s Biomimetic MicroElectronic Systems (BMES) Engineering Research Center, reported on an experimental system that includes a 1000-pixel test chip. He expects to have the high-res retina at a point where they can begin clinical trials in about five years.


In the artificial retina, a camera mounted on glasses outside the eye sends the visual signals to two RF coils inside the front half of the eye. An electronics module inside the eye’s vitreous humor—the gelatinous saline sac that fills the space between the lens of the eye and the retina at the back of the eye—translates the RF signals into voltages for use in the high-res retina chip. Lying against the retina is a grid of 1000 electrodes on a flexible substrate; these electrodes apply voltage signals to the retina, which interprets them as photons. The rest of the visual process takes place as usual, and the system mimics relatively normal vision.


The group, which includes researchers from the BMES center, the California Institute of Technology, in Pasadena, and the University of California, Santa Cruz, which developed earlier prototypes in collaboration with Second Sight Medical Products. The first was the Argus 16, with 16 electrodes; the next, Argus II, has 60. Both have been in clinical trials. The Argus II implant enabled blind clinical-test subjects to follow a straight line for about 6 meters without deviating from the path. But the key to a medical device’s ability to grant true independence is whether it allows the person to identify faces or read. Artificial-eye researchers estimate that such tasks will require between 600 and 1000 electrodes.


Ideally, that artificial retina would be contained entirely within a person’s eyeball. In order to create a fully self-contained high-resolution system, the team must consider many different pieces: a parylene coating to protect the prosthesis from the corrosive effects of being inside the body for 60 years or more, a flexible substrate that can conform to the idiosyncracies of different individuals’ retinal curves, and, most important, wireless power. 


Instead of batteries, the device uses inductive coils that pick up energy transmitted from outside the body. The researchers are also relying on insights from MEMS fabrication: the implant coils, interconnects, and 1000 electrodes are formed during a single parylene micromachining process.


“This is a really breathtaking system,” says MIT electrical engineering professor Jesus del Alamo, who organized the panel at IEDM where Weiland discussed the group’s research. “They have every piece of the system in place—they have even designed their own software.” 


But there is more work to be done. “You need to get everything into the eye,” says Jamal Deen, a professor of electrical and computer engineering at McMaster University, in Ontario, “including the camera.”


So far, the camera, image-processing hardware, power amplifier, and data modulator are external, but Weiland hopes to implant even the camera part of the system by fixing it to the lens of the eye. His collaborators at USC are working on miniaturizing the camera system so that it can be placed onto the lens in a routine surgical procedure similar to cataract surgery. “If we can make a camera the size of the lens, we can implant it there,” he says. “But again, the challenge is making a self-contained camera without a larger control circuit.”


He cautions that it will take several years to put the whole system together and start clinical trials. But those trials will lean heavily on what is learned from trials of the implant being tested today. So potential patients should not wait for the new chip. “The 1000-channel device is likely more than five years away from even starting clinical testing,” says Weiland. “In the meantime, our 60-channel device has been in clinical trials for over two years, and sometimes we run into difficulty recruiting for the trial because some prospective participants are aware of the research efforts on higher-channel-count devices.”