Dr. Grossman’s Blog

Image by Roman Pavlyuk

“Geographic atrophy,” which causes cell death in the retina of the eye, is blamed as a major cause of what is often described as untreatable blindness.  It is associated with dry macular degeneration, a disease that affects over 10 million Americans.

Researchers publishing in the journal Nature find a DNA level cause for macular degeneration: non-coding “junk DNA” that was previously thought to have no function.  The scientists also found that another genetic component, RNA in a toxic form called Alu RNA, is also involved in retinal cell death.

These two discoveries could open new doors for therapies for macular degeneration patients.  Source: http://www.medicalnewstoday.com/articles/215812.php

Learn more about how to prevent and treat macular degeneration naturally.

Often, patients suffering from macular degeneration will use a different part of their retinas to make up for central vision loss. According to researchers from Georgia Tech’s School of Psychology, the brains macular degeneration patients can also compensate to vision changes by reorganizing their neural connections.

Using functional MRI technology, researchers found that even though study participants were relying on their peripheral vision rather than their central vision, the brain was actually processing information as if the patients had normal, unimpeded vision.

Study leader Eric Schumacher told Science Daily: “Our results show that the patient’s behavior may be critical to get the brain to reorganize in response to disease.  It’s not enough to lose input to a brain region for that region to reorganize; the change in the patient’s behavior also matters.”  This “behavior change” is the macular degeneration patient’s ability to compensate for central vision loss by relying on other areas of the visual field.

Source: EyeWorld News Magazine

Visit our website for self help tips specifically for macular degeneration sufferers.

Two research studies have shown that defects in a gene that is an important regulator of parts of the immune system can significantly increase the risk of the age-related macular degeneration (AMD).  While one group of scientists identified the harmful variation of the gene that was linked to the development of AMD, another group identified a another variant possessed by 20 percent of the population that can actually protect people against AMD. Work is being done to find a way to combat AMD with the help of this particular protective protein.

Source: http://www.technologyreview.com/biomedicine/25386/?ref=rss&a=f

Researchers have found that cataract surgery is not associated with an increased risk of age-related macular degeneration (AMD) progression in patients with non-neovascular AMD.

Surgeons enrolled 108 patients with nonneovascular AMD who were awaiting cataract surgery. Fluorescein angiography was performed preoperatively, and again at postoperative week 1, month 3, and month 12 visits.

After 12 months, neovascular AMD developed in only 3 of 65 eyes (4.6%) that did not have neovascular AMD at the preoperative visit or the one-week postoperative visit.  This statistic is consistent with an estimated one-year progression rate in the general AMD population.

Results of this study, published in the November issue of the Archives of Ophthalmology, state that the low incidence of neovascular AMD development between 1 week and 1 year after cataract surgery did not support the hypothesis that cataract surgery increases the risk of AMD progression.

Researchers also noted that  several eyes appeared to have disease progression on postsurgery week 1 fluorescein angiograms, suggesting that many cases of presumed progression to neovascular AMD following cataract surgery may have been present prior to cataract surgery, but not recognized owing to lens opacity.

Read other studies about macular degeneration at the Natural Eye Care site

SOURCE:  Progression of Age-Related Macular Degeneration After Cataract Surgery, Dong, et al, Arch Ophthalmol. 2009;127(11):1412-1419.

People with age-related macular degeneration (AMD) who are taking anticoagulant and antiplatelet drugs such as aspirin, warfarin, and clopidogrel run a significant risk of retinal hemorrhage.  

A study presented at the Retina Congress 2009 reviewed the records of 195 eyes in 195 patients, average age 83, of whom 96 were taking antiplatelets and anticoagulants on a daily basis.

Of the patients taking antiplatelets or anticoagulants, 63% developed retinal hemorrhage compared with 29% who were not taking these drugs.  It is estimated that 7.6 patients out of 100 would develop retinal hemorrhage each year when taking these drugs.  The risk of retinal hemorrhage was highest among patients who were using multiple drugs.

Since taking the patient off the blood-thinning agent is not an option, study authors suggest that ophthalmologists follow these patients closely.  It is recommended that information about a patient’s use of antiplatelets and anticoagulants should be noted prominently on the patients’ charts.

The 2009 Retina Congress is a combined meeting of the American Society of Retina Specialists, the Macula Society, and the Retina Society.

Source:  “The Association of Antiplatelets and Anticoagulants With Intraocular Hemorrhage in Patients With Exudative Age-Related Macular Degeneration,” http://www.asrs.org/

Researchers at Washington University School of Medicine in St. Louis have identified an intricate process that allows the human eye to adapt to darkness very quickly, as well as the process by which the eye can function in bright light.

This research will help scientists better understand human diseases that affect the retina, including age-related macular degeneration (AMD).

The retina’s main light-sensing cells are called rods and cones.   Cone cells allow us to see colors and can adapt to rapid changes in light intensity.   Cones use light-sensing molecules that bind together to make up visual pigments which are destroyed when they absorb light.  They must be rebuilt, or recycled, for the cone cells to continue sensing light. After exposure to light, key components of pigments called chromophores can leave the cells and travel to the nearby pigment epithelium near the retina. There the chromophore is restored and returned to the photoreceptor cells.

Researchers removed the pigment epithelium layer in salamander retinas, so that pigment molecules could not be recycled that way.  When they exposed retinal cells both to bright light and to darkness they found that the rods no longer worked, but the cones continued to function properly, even without the eye’s pigment epithelium.

Scientists treated mouse retinas with a chemical that destroyed Müller cells, which support and interact with rods and cones.  The retinas were then exposed to bright light, followed by darkness.   

When the function of Müller cells was blocked the retinal visual pathway could not function because cones ran out of photopigment and could not adapt to dark. When the Müller cells function properly, cones in the mouse, primate and human retinas are able to function in bright light and adapt to darkness, independently of the pigment epithelium.

Study authors believe that in the future it may be possible to manipulate this pathway in the retina to improve vision when the other pathway, involving pigment epithelium, has been interrupted by injury or disease, such as age-related macular degeneration.

SOURCE:  Wang, et al, “An alternative pathway mediates the mouse and human cone visual cycle”, Current Biology vol. 19 (19), Oct. 13, 2009.
“Researchers discover mechanism that helps humans see in bright and low light”, http://mednews.wustl.edu/news/page/normal/14856.html

Researchers at the University of Wisconsin have successfully grown light-sensing retinal cells from human skin cells. 

The ability to grow retinal cells may someday be used to treat degenerative eye diseases such as macular degeneration and retinitis pigmentosa by enabling doctors to repair damage to the retina with new cells generated from the patient’s skin.

Scientists at the University of Wisconsin manipulated human skin cells to act like embryonic stem cells, which can be used to grow into any tissue in the body. 

The study, published in the journal Proceedings of the National Academy of Science, indicates that the ability to create human retinal cells helps researchers better understand how eyes develop, enabling them to better treat genetic eye conditions.

SOURCE:  Modeling early retinal development with human embryonic and induced pluripotent stem cells, Meyer, et al, Proceedings of the National Academy of Science, http://www.pnas.org/content/early/2009/08/24/0905245106.abstract

Oral supplementation with lutein and zeaxanthin with coantioxidants may improve vision at 36 months for those at high risk for progression to late age-related macular degeneration (AMD).

In the Carotenoids and Co-Antioxidants in Age-Related Maculopathy (CARMA) study, presented at the Association for Research in Vision and Ophthalmology (ARVO) 2009 Annual Meeting, researchers examined the effects of supplementation with serum lutein and zeaxanthin plus coantioxidants (vitamins C and E and zinc) on visual function and the progression from early to late stages of AMD.

A total of 433 participants in the United Kingdom with early AMD in at least one eye, or any level of AMD in the study eye and late-stage AMD in the fellow eye, received either carotenoids plus coantioxidants or a placebo.

Study participants were examined at 12, 18, 24, 30, and 36 months. Although no statistically significant difference was seen in best corrected distance visual acuity (BC DVA) at 12 months, at the 36 month follow-up researchers did note an improved BC DVA.

Investigative team member Usha Chakravarthy, MD, PhD, from Queens University of Belfast in Northern Ireland concluded that supplementation with lutein and zeaxanthin results in better macular function in patients with early AMD. He also noted that the eyes of people who had high serum (lutein) demonstrated a less severe early AMD change over time, and suggested that supplementation may prove beneficial in preventing progression to late AMD.

Learn about self-help for macular degeneration, including recommended diet and supplements containing lutein and zeaxanthin at the Natural Eye Care website

SOURCE: ARVO 2009: Lutein, Zeaxanthin Supplements May Result in Better Macular Function in Early AMD, Chakravarthy, et al, The Association for Research in Vision and Ophthalmology (ARVO), May 4, 2009.

Researchers at the University of North Carolina at Chapel Hill School of Medicine and the University of Kentucky have identified a new target for the diagnosis and treatment of age-related macular degeneration.

In a study published by the journal Nature, researchers demonstrate that blocking the activity of a specific protein, called CCR3, can reduce the abnormal blood vessel growth that leads to macular degeneration. Targeting this new protein may prove to be safer and more effective than the current treatment for the disease, which is directed at a protein called vascular endothelial growth factor or “VEGF.”

When researchers blocked CCR3, either with drugs or through genetic engineering, they saw a decrease in the generation of abnormal blood vessels. Drugs targeting CCR3 were significantly more effective than those targeting VEGF, which could represent a new therapy for the two-thirds of patients who do not respond to current treatment.

Study authors hope that this discovery may enable physicians to catch the disease in its earliest stages, before blood vessels have fully infiltrated and destroyed the central portion of the eye’s retina (the macula) to cause vision loss.

“It would be much better to prevent the disease in the first place,” said study co-author and principal investigator of the UNC study site, Mary Elizabeth Hartnett, M.D., a professor of ophthalmology in the UNC School of Medicine. “An exciting implication of this study was that the CCR3 protein could be detected in early abnormal blood vessel growth, giving us the opportunity to prevent structural damage to the retina and preserve vision.”

Learn more about macular degeneration at the Natural Eye Care web site

Read other studies about macular degeration

Source: Study suggests new approach to common cause of blindness, Hartnett, et al, June 14, 2009, href=”http://www.unchealthcare.org/site/newsroom/news/2009/June/hartnett?searchterm=macular+degeneration

Patients with age-related macular degeneration (AMD) experience a deterioration of their central vision. Two thirds of AMD patients have problems with visuomotor and balance skills resulting in clumsiness and increased risk of falls.

A new study investigates the link between balance training and improved visual, vestibular and somatosensory functions involved in balance control. The investigation, published in the Journal of Vestibular Research, measured the impact of balance training on several visuomotor functions and reading speed.

Balance status statistics of 54 AMD patients were compared to 55 normal controls. Sixteen of these patients and 14 controls subsequently received balance training sessions on a postural platform. Researchers assessed postural sway, pointing accuracy, reading performance and, for the AMD patients, the effect of low vision training and balance training on the shift from several spontaneous Preferred Retinal Loci (PRLs) to one or more Trained Retinal Loci (TRL).

Even after a limited number of sessions of cross-modal balance training, the results show a significant improvement for the vestibular input and fixation stability, leading to the conclusion that more training sessions may help AMD patients gain more significant improvement of visuo-motor functions.

Learn more about AMD, including diet, nutrition, self-help and alternative treatment information at the Natural Eye Care website

Read other studies on AMD prevention and treatment options

SOURCE: Balance training and visual rehabilitation of age-related macular degeneration patients, Radvay, et al, Journal of Vestibular Research, Volume 17, Number 4, 2007, pages 183 – 193.