Relationship Between Glaucoma and Diabetes, Hypertension

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Posted on 9th September 2011 by Pacific ClearVision Institute in Retina

Many Americans suffer from diabetes and hypertension and, according to a study by researchers at the University of Michigan Kellogg Eye Center, these individuals may have an increased risk of developing open-angle glaucoma (OAG).

Joshua D. Stein, M.D., M.S., a glaucoma specialist at Kellogg, led a research team that recently reviewed billing records of more than 2 million people aged 40 and older who were enrolled in a managed care network in the United States and who visited an eye care provider one or more times from 2001 to 2007. The researchers found that people with diabetes alone had a 35 percent increased risk of developing OAG and those with hypertension alone had a 17 percent increased risk. For people with both diabetes and hypertension, there was a 48 percent increased risk of developing OAG, the most common form of glaucoma in the country.

The study focused on the possible associations between various components of metabolic syndrome — a collection of conditions that includes obesity, hypertension, diabetes, and hyperlipidemia (high cholesterol and high triglyceride levels) — that affects one fifth of the U.S. population. The Kellogg researchers also examined how each component increased or decreased the risk of glaucoma.

While the researchers found that diabetes and hypertension increased the risk of OAG, the study showed that hyperlipidemia actually reduced by 5 percent the risk for developing the disease. Further research is under way to evaluate whether it is the hyperlipidemia itself, the medications used to treat the condition, or both that reduces the risk of glaucoma. Findings from this research may eventually lead to novel treatments for glaucoma.

“Patients who have diabetes and hypertension are already known to be at elevated risk for eye conditions like diabetic retinopathy, a condition that harms the blood vessels in the retina,” says Dr. Stein. “This study and others suggest that, for these patients, an increased likelihood of glaucoma is also a concern.”

Glaucoma is a leading cause of irreversible blindness worldwide. In the United States, more than 2.2 million individuals have this disease. And, as the U.S. population ages, glaucoma diagnoses are expected to increase. Because OAG symptoms usually don’t surface until the disease has progressed, understanding the risks associated with OAG — elevated intraocular pressure, positive family history of glaucoma, increased age and non-white race — will help physicians identify which patients would benefit most from screening and monitoring.

“This study reinforces the importance of regular eye examinations for patients at increased risk of glaucoma, including those with diabetes and hypertension,” says Dr. Stein. ”

The study was funded by the National Eye Institute.

Aging Eyes Linked to Sleepless Nights, New Study Shows

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Posted on 9th September 2011 by Pacific ClearVision Institute in Retina

A natural yellowing of the eye lens that absorbs blue light has been linked to sleep disorders in a group of test volunteers, according to a study in the September 1 issue of the journal Sleep. As this type of lens discoloration worsened with age, so did the risk of insomnia.

“The strong link between lens yellowing and age could help explain why sleep disorders become more frequent with increasing age,” said Line Kessel, M.D., Ph.D., the study’s lead author.

In the Danish study, 970 volunteers had their eyes examined by lens autofluorometry, a non-invasive method for determining how much blue light is transmitted into the retina. Blue light is a portion of the visible-light spectrum that influences the normal sleep cycle by helping initiate the release of melatonin in the brain. Melatonin is a hormone that helps signal to the body when it is time to be sleepy or alert.

Volunteers were considered to have a sleep disorder if they confirmed that they “often suffer from insomnia” or if they purchased prescription sleeping pills within the last 12 months. Of those classified as having a sleep disturbance, 82.8 percent affirmed that they both suffered from insomnia and used sleep medication.

Using this data, researchers calculated an inverse relationship between blue light transmission and the risk of having sleep disturbances: the lower the blue light transmission into the retina due to a yellowing of the eye lens, the greater the risk of sleep disturbances.

“The results showed that while age-related lens yellowing is of relatively little importance for visual function, it may be responsible for insomnia in the elderly,” said Kessel, a senior scientist in the Department of Opthalmology at Glostrup Hospital in Denmark.

Significantly higher rates of sleep disorders were reported by older participants, women, smokers and those with diabetes mellitus. Previous studies have shown that the rate of lens aging is accelerated in smokers, patients with diabetes mellitus and those at high risk for ischemic heart diseases. The Danish researchers addressed these factors in their statistical analyses.

“The association between blue light lens transmission and sleep disturbances remained significant even after we corrected for age, sex, diabetes mellitus, smoking and the risk of ischemic heart disease,” Kessel said.

She said another important factor to consider is that sleep quality has been shown to improve after cataract surgery. “The transmission of blue light currently cannot be improved by any other method than cataract surgery. I´m involved with another research project where we try non-invasively to remove the yellow color of the lens using a laser, but the method is not yet developed for clinical use,” Kessel said.

In the meantime, Kessel said it seemed prudent to recommend that physicians reconsider the prescription of sleeping tablets in patients who have undergone cataract surgery.

Sight Fails When Defective Eye Cells Cripple Renewal

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Posted on 9th September 2011 by Pacific ClearVision Institute in Retina

In a rare eye disease, the retina degenerates because light-receiving cells fail to regenerate, research led by a student at Case Western Reserve University School of Medicine shows.

The researchers include Dr. Samuel G. Jacobson’s group at the University of Pennsylvania and Dr. Andreas Engel’s group at University of Basel, Switzerland. They found that when the natural renewal process fails, metabolites are locked in, build up and turn toxic, killing cells over time in Enhanced S-Cone Syndrome.

A description of their work is online and will be published in print in the Journal of the Federation of American Societies for Experimental Biology on September 1.

The discovery provides a target to treat and prevent blindness caused by the disease, also known as Goldmann-Favre Syndrome, which is found in about one in 1 million people.

But, more importantly the researchers say, the findings and the scientists’ use of two technologies to uncover the mechanisms leading to sight loss may help gain understanding of a broad array of retinal degenerative diseases, including macular degeneration, affecting millions worldwide.

“Although rare, Enhanced S-Cone Syndrome helps us understand critical visual processing errors that arise in disease,” said Debarshi Mustafi, who is earning his medical degree and PhD in pharmacology at Case Western Reserve. He is lead author of the study. “Knowing that photoreceptor cells affect their own renewal will surely have an impact on other, more common, forms of retinal degeneration.”

Enhanced S-Cone Syndrome is a condition in which the eye no longer has an orderly balance of cells called rods and cones, which enable us to see lights of different wavelengths, that is, different colors. Instead, cones that receive short wavelength light dominate and are clumped throughout the retina.

Those with the disease become night blind and progressively develop blind spots and lose sight as they age, until reaching blindness.

Genes connected to the disease have been known for some time. To find the molecular mechanism that causes sight loss, the researchers examined mouse models of the disease and 9 patients with the syndrome.

Optical imaging of the patients over a decade revealed an abnormal interface between the cones and the adjacent layer of tissue, called the retinal pigment epithelium.

Using gene-sequencing techniques on the mouse models, the team found expression of 30 genes involved in sight differed in healthy mice versus the disease models. Three of the genes were engaged in renewal of photoreceptors, a process called phagocytosis.

The researchers used a scanning electron microscope to produce images down to 100 nanometers, or the size of the largest holes in a surgical mask.

They found no phagosomes, essentially compartments made in cone cell membranes in which specialized cells called phagocytes of the retinal pigment epithelium eat cone material. In a healthy retina, phagosomes are present; phagocytes eat about 10 percent of the cone per day, continually renewing the cone.

The images instead showed bulbous cones in which metabolites that would normally be consumed remain, causing the swelling and turning toxic, the researchers said.

Analysis of cell cultures confirmed aberrations in the cones themselves were the cause of the problem, not the adjacent pigment layer as was previously thought.

“What we learn from this inherited human disease, and its mouse model, will be helpful to understand the aging process of the retina, like that seen in age-related macular degeneration,” said Krzysztof Palczweski, John H. Hord Professor and chair of the Department of Pharmacology at CWRU School of Medicine. Palzcweski is Mustafi’s advisor and senior author of the paper. “It is very likely that the phagocytotic process described in Debarshi’s paper is a dysfunction as we age.”

Mustafi said the methods that led to the discovery — combining gene sequencing and imaging — may have a wider impact. “It is a new way to study any disease.”

Researchers Identify Gene That Leads to Myopia (Nearsightedness)

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Posted on 9th September 2011 by Pacific ClearVision Institute in Retina

A Ben-Gurion University of the Negev research group led by Prof. Ohad Birk has identified a gene whose defect specifically causes myopia or nearsightedness.

In an article appearing online in the American Journal of Human Genetics, Birk and his team reveal that a mutation in LEPREL1 has been shown to cause myopia.

“We are finally beginning to understand at a molecular level why nearsightedness occurs,” Prof. Birk says. The discovery was a group effort at BGU’s Morris Kahn Laboratory of Human Genetics at the National Institute for Biotechnology in the Negev and the Dayan Clinical Genetics Wing at Soroka University Medical Center.

Nearsightedness is the most common human eye disorder and is mostly a hereditary trait. Aside from being a significant public health concern, nearsightedness also leads to a higher incidence of other secondary eye disorders, such as retinal detachment, macular degeneration, as well as early onset glaucoma and cataracts. Despite decades of intensive research, the specific genes whose defects lead to nearsightedness have remained elusive.

The defective gene was identified in a thorough study of severe early-onset myopia that is common in a specific Bedouin tribe in southern Israel. As part of the research and in collaboration with a Finnish group, studies in a model system using insect cells demonstrated that the mutation is detrimental to the enzymatic activity of the gene.

The gene, LEPREL1, encodes an enzyme that is essential for the final modification of collagen in the eye. In the absence of the active form of this enzyme, aberrant collagen is formed, causing the human eyeball to be longer than normal. As a consequence, light beams entering the eyeball focus in front of the retina rather than on the retina itself and myopia emerges.

Future studies will determine whether LEPREL1 or its related genes play a significant role in the causation of myopia in the population at large as well.

Prof. Birk’s group has thus far elucidated the molecular mechanisms leading to more than 15 human diseases, and the research findings are effectively implemented in massive screening tests and prevention programs.

Scientists Unravel the Cause of Rare Genetic Disease: Goldman-Favre Syndrome Explained

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Posted on 9th September 2011 by Pacific ClearVision Institute in Retina

A new research report published in The FASEB Journal will help ophthalmologists and scientists better understand a rare genetic disease that causes increased susceptibility to blue light, night blindness, and decreased vision called Enhanced S-Cone Syndrome or Goldman-Favre Syndrome. In the report, scientists found that the expression of genes responsible for the healthy renewal of rods and cones in the retina was reduced and that this problem originates in the photoreceptors themselves rather than in the adjacent retinal pigment epithelial layer as once thought.

“This research could help identify therapeutic agents that would prevent, ameliorate or possibly cure these blinding diseases related to defective renewal of retinal cells,” said Krzysztof Palczewski, Ph.D., a senior scientist involved in the research and an editorial board member of The FASEB Journal from the Department of Pharmacology in the School of Medicine at Case Western Reserve University, in Cleveland, Ohio. “It is possible that during aging, this process is slowed and such intervention could be important for determining diseases such as age-related macular degeneration.”

To make this discovery, researchers studied both human ESCS patients and an ESCS mouse model. They found that phagocytosis, a process that allows for the normal and continual renewal of rods and cones in the retina, was defective. Using RNA-sequencing to identify differences in complete transcriptomes, and cell culture techniques, scientists demonstrated that the phagocytotic defect was due to the ESCS photoreceptors themselves, rather than the adjacent retinal pigment epithelium layer that also is involved in photoreceptor phagocytosis.

“Learning what goes wrong in rare diseases like Enhanced S-Cone Syndrome allows us to understand how vision works at the molecular level,” said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “This study provides valuable insight into how the eye renews its photoreceptor cells. Knowing that photoreceptor cells affect their own renewal will surely have an impact on other, more common, forms of retinal degeneration.”

According to the U.S. National Institutes of Health Office of Rare Diseases, Enhanced S-Cone Syndrome is an inherited eye disease that affects the retina. Within the retina are “red,” “blue,” and “green” cones allowing people to see colors properly; and rods which allows us to see in dim light. People with Enhanced S-Cone Syndrome are born with an overabundance of blue cones, reduced numbers of red and green cones, and few, if any, functional rods. This leads to an increased sensitivity to blue light, varying degrees of red and green cone vision, night blindness occurring from early life, vision loss, and retinal degeneration.