all ophthalmology stories

Bacterium present in eyes with 'wet' age-related macular degeneration

70652986 — Mon, 26 Mar 2007 06:23:08 -0400

Age-related macular degeneration (AMD) is the leading cause of blindness in Americans over the age of 55. The majority of vision loss is due to neovascular AMD, the advanced form of the disease characterized by the formation of blood vessels in the macula, the center part of the eye's retina. These blood vessels often leak, thus giving neovascular AMD the name of "wet" AMD.

Researchers at the Massachusetts Eye and Ear Infirmary (MEEI) have found that chlamydia pneumoniae, a bacterium linked to heart disease and capable of causing chronic inflammation, was present in the diseased eye tissue of five out of nine people with "wet" AMD. However, it was not found in the eyes of more than 20 individuals without AMD, providing more evidence that this disease may be caused by inflammation. The study is described in the November 2005 issue of Graefe's Archive for Clinical and Experimental Ophthalmology.

"The paper showed that C. pneumoniae is capable of modifying the function of important cell types involved in regulating normal eye function," said lead author Murat Kalayoglu, MD, PhD. "We found that C. pneumoniae infection led to increased production of vascular endothelial growth factor (VEGF), the key protein involved in wet AMD. That C. pneumoniae infection of human eye cell types increases VEGF production is therefore significant and could explain in part why VEGF levels are increased in many people with wet AMD." Kalayoglu is a Harvard Medical School research fellow in ophthalmology at MEEI.

Study shows new compound may reduce risk of vision loss in patients with diabetes

70652986 — Mon, 26 Mar 2007 06:21:31 -0400

The PKC-Diabetic Retinopathy Study (DRS) was designed to evaluate the safety and effect of an oral treatment, RBX, on retinopathy progression or visual loss in patients with moderately severe to very severe nonproliferative diabetic retinopathy. In the study, patients with type 1 or type 2 diabetes received either RBX or a placebo over three to four years. The study measured the effect of three orally administered doses of RBX on progression of diabetic retinopathy, moderate visual loss and sustained moderate visual loss. The study was conducted at Joslin Diabetes Center and assorted national and international medical centers.

The oral treatment RBX inhibits the activity of the enzyme protein kinase C. PKC is essential to the normal production of energy in the body, but one form of the enzyme - PKC-beta - has been linked to diabetic complications of the eye and other parts of the body. Thus RBX was designed to be selective for the single PKC-beta isoform.

"Our results demonstrate that although RBX did not prevent progression to proliferative diabetic retinopathy, it may reduce the risk of moderate vision loss caused by macular edema," said study chairman Lloyd Paul Aiello, M.D., Ph.D., head of Joslin's section on eye research, director of Joslin's Beetham Eye Institute and associate professor of ophthalmology at Harvard Medical School.

Schepens scientists regenerate optic nerve for the first time

70652986 — Mon, 26 Mar 2007 06:20:43 -0400

In earlier research, Dr. Dong Feng Chen, lead author of the study, assistant scientist at Schepens Eye Research Institute and an assistant professor of ophthalmology at Harvard Medical school, and her team discovered several processes that they believed "locked up" the optic nerve's ability to regenerate. The first lock was the turning off of the gene BCL-2, which, when turned on, activates growth and regeneration. The second lock, they theorized, was a scar on the brain created shortly after birth by "glial" cells.

In the current research, Dr. Kin-Sang Cho, research associate in Chen's laboratory and the first author of the paper, tested two keys to unlock regeneration. The first key involved the development of a mouse model in which the BCL-2 gene is always turned on (or is over-expressing). The second key was the use of a mouse line carrying mutations of "glial specific genes" that lead to the reduced "glial scar" formation.

Unlocking the regeneration with the first key caused robust optic nerve regeneration, but only in the mice whose brains had not yet formed a "glial scar."

Cho then added the second key by combining BCL-2 over- expresser with the "glial gene" mutation to prevent the development of the "glial scar" in the older transgenic mice. He found that this combination caused rapid, robust regeneration of the optic nerve again, as with the younger mice.

The next step for Chen and her colleagues is to determine if the regenerated optic nerves were functional.

Hormone replacement therapy may lower degenerative eye disease risk in postmenopausal women

70652986 — Mon, 26 Mar 2007 05:26:32 -0400

ARM is a degenerative eye disease that affects the macula, which is responsible for central vision, which is necessary for reading, driving and recognizing people's faces. Advanced ARM is the leading cause of irreversible blindness among elderly individuals worldwide. Approximately 1.7 million people have decreased vision due to ARM, and 200,000 people develop advanced ARM with visual loss each year. A study published in the December 2002 issue of the American Journal of Ophthalmology showed that postmenopausal hormone therapy may reduce the risk of having advanced ARM among women with signs of maculopathy. "Decisions regarding postmenopausal hormone therapies are becoming increasingly complex, and it is important to evaluate their effects, including testing their relationship to eye diseases of aging," said lead author Johanna M. Seddon, director of the Epidemiology Unit at the Massachusetts Eye and Ear Infirmary and associate professor of ophthalmology at Harvard Medical School.

Researchers eye earliest triggers of age-related macular degeneration

70652986 — Mon, 26 Mar 2007 05:18:53 -0400

Age-related macular degeneration is the leading cause of blindness for Americans over 60 years of age. It affects more than 14 million people. But how it attacks the macula, the center of the retina, is a controversial question. The macula is where the cones -- the color and light sensing cells of the eye -- reside. Macular degeneration involves the decreased functioning of the cones. Some researchers have long thought that the demise of the cones involves the inability of the cones to regenerate a necessary pigment. But a more complicated picture is emerging because of the work of Harvard researchers. Schepens Eye Research Institute's Ann Elsner, Stephen Burns, and John Weiter have been studying people with early stages of disease and found that the cones' ability to collect light is impaired even when their ability to regenerate pigment is about normal. The researchers, whose report appears in the January 2002 Journal of the Optical Society of America, suggest that the initial problem lies not in the cones' ability to recycle their light-processing pigment but in their ability to physically capture light in the first place. The findings could be used to prevent future generations from suffering macular degeneration's damage.

Snack foods may increase risk of age-related sight loss

70652986 — Mon, 26 Mar 2007 05:15:26 -0400

Macular degeneration results from the malfunctioning or loss of function of photo-sensitive cells in the retina. According to the Macular Degeneration Foundation, more than 13 million people in the United States are affected; a new case of adult macular degeneration is diagnosed in the U.S. every three minutes. A study in the August 2001 issue of the Archives of Ophthalmology found that a higher intake of specific types of fat, including vegetable, monounsaturated and polyunsaturated fats, may be associated with a greater risk for advanced adult macular degeneration.

Sights set on partial corneal transplants

70652986 — Mon, 26 Mar 2007 05:04:23 -0400

"We don't have any way of curing these problems," says Nancy Joyce, a Harvard researcher who is working on saving people's sight when their corneas deteriorate. "The only way right now is full corneal transplantation, healthy tissue and all. In our work, we're trying to facilitate replacement of the diseased tissue only." To do that, she's working with colleagues who are generating new cells from old ones. Early results suggest cell transplants may be possible. "We're probably talking somewhere between 5 and 10 years before clinical trials," Joyce said. "We're still in the very early stages."