Vitamin B-Based Treatment for Corneal Disease May Offer Some Patients a Permanent Solution

Vitamin B-Based Treatment for Corneal Disease May Offer Some Patients a Permanent Solution.

ScienceDaily (Oct. 24, 2011) - Patients in the United States who have the Cornea-damaging disease keratoconus may soon be able to benefit from a new treatment that is already proving effective in Europe and other parts of the world. The treatment, called collagen crosslinking, improved vision in almost 70 percent of patients treated for keratoconus in a recent three-year clinical trial in Milan, Italy. The treatment is in clinical trials in the United States and is likely to receive FDA approval in 2012.

The results of the Milan study are being presented Oct. 24, 2011 at the 115th Annual Meeting of the American Academy of Ophthalmology in Orlando, Florida.
In a session titled Long-term Results of Corneal Crosslinking for Keratoconus, Paolo Vinciguerra, MD will describe the treatment and three-year follow up of more than 250 keratoconus patients who received collagen crosslinking at his clinic. Sixty-eight percent of the 500 eyes treated gained significant visual acuity, with their results remaining stable at the end of the follow-up period. Patients over age 18 were most likely to improve.
In the collagen crosslinking procedure, riboflavin (vitamin B) is applied to the Cornea, which is then exposed to a specific form of ultraviolet light. Collagen fibers regenerate with new bonds forming between them, increasing Corneal stiffness and strength. The treatment also combats the causes of keratoconus, reducing the chance that it will recur. The rest of the eye receives only minimal UV exposure during treatment. Dr. Vinciguerra's new study confirms that adverse effects are rare. Previous research by his team indicated no loss of Corneal endothelial cell, a measurement used to assess the safety of corneal treatments, in patients who received collagen crosslinking.
"For many people with keratoconus, collagen crosslinking can provide a better and more permanent solution to their vision problems," said Dr. Vinciguerra. "Given that no current treatment in use in the U.S. offers permanent correction, this effective option represents a significant advance for corneal medicine."
One in 2,000 people in the United States and worldwide are diagnosed with keratoconus, a disease that damages the collagen fibers that form the structure of the cornea, which is the outer surface of the eye. The cornea's crucial task is to focus, or "refract," incoming light toward the eye's lens. To perform properly, the cornea needs to be rounded, like the surface of a ball. As keratoconus worsens and the cornea becomes thinner, it may bulge outward in a cone shape, causing nearsightedness and/or astigmatism, making clear vision impossible. As the number of fibers and links between them decline, the cornea loses up to 50 percent of its normal stiffness.
Standard treatments in the U.S., such as specialized eyeglasses, contact lenses, or implanted lenses, cannot permanently correct keratoconus, and none of these treatments address the underlying causes. Severe keratoconus often requires corneal transplant.
The 115th Annual Meeting of the American Academy of Ophthalmology is in session October 23 through 25 at the Orange County Convention Center in Orlando, Fla. It is the world's largest, most comprehensive ophthalmic education conference. Approximately 25,000 attendees and more than 500 companies gather each year to showcase the latest in ophthalmic technology, products and services. To learn more about the place Where All of Ophthalmology Meets visit www.aao.org/annual_meeting.

http://www.sciencedaily.com/releases/2011/10/111024084641.htm
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How Does Nearsightedness Develop in Children?

How Does Nearsightedness Develop in Children?

ScienceDaily (Mar. 1, 2012) - Myopia (Nearsightedness) develops in children when the lens stops compensating for continued growth of the eye, according to a study in the March issue of Optometry and Vision Science, official journal of the American Academy of Optometry.

The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.
Using detailed information on eye growth and vision changes in children over time, the new research shows "decoupling" of lens adaptation from eye growth about a year before myopia occurs. Donald O. Mutti, OD, PhD, of The Ohio State University College of Optometry, is lead author of the new study.
Growth Imbalance Leads to Myopia…
The researchers analyzed repeated measurements of vision and eye growth performed over several years in children aged 6 to 14. The study focused on the growth of the two key parts of the eye affecting normal vision: the cornea, the transparent front part that lets light into the eye; and the lens, located behind the cornea, which focuses light rays on the retina at the back of the eye.
Myopia or Nearsightedness -- difficulty seeing objects at a distance -- develops in about 34% of American children as they grow. Vision professionals and scientists typically think of myopia as a problem occurring when the eyeball becomes too long (front to back) for the optical power of the cornea and lens.
However, it has been unclear how this imbalance develops in children who previously had normal vision. To answer this question, Dr. Mutti and colleagues compared changes in eye growth for children who developed myopia at different ages versus those whose vision remained normal.
They found that, in children without myopia, the lens grew thinner and flatter to maintain normal vision as the eye grew. This adaptation maintained a normal balance between the optical power of the lens and the increasing length of the eyeball. From age nine months to nine years, eyeball length increased by an average of three millimeters.
...As Lens Stops Responding to Increasing Eye Length
However, in children who developed myopia, the lens stopped changing in response to eye growth. Nearsightedness developed not just because of increases in the length of the eyeball, but rather because the optical power of the lens no longer changed as the eye grew.
The imbalance occurred rather suddenly: about one year before the children became Nearsighted. For at least five years after the development of myopia, the eye kept becoming longer but the lens stopped flattening and thinning.
In contrast to the lens, changes in corneal growth showed little or no relation to the development of myopia. The cornea is responsible for about two-thirds of the optical power of the eye, and the lens for the remaining one-third.
The study provides vision professionals with an important new piece of information on why some children develop myopia. However, what's still unclear is why the lens suddenly stops adapting to continued growth of the eye. More research will be needed to answer that question -- one possibility is that an abnormally thick ciliary muscle within the eye forms a mechanical restriction preventing the stretching that thins and flattens the lens as the eye continues to grow.
http://www.sciencedaily.com/releases/2012/03/120301113258.htm
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Study Links Genes to Common Forms of Glaucoma.

Study Links Genes to Common Forms of Glaucoma

ScienceDaily (Apr. 26, 2012) - Results from the largest genetic study of Glaucoma, a leading cause of blindness and vision loss worldwide, showed that two genetic variations are associated with primary open angle Glaucoma (POAG), a common form of the disease. The identification of genes responsible for this disease is the first step toward the development of gene-based disease detection and treatment.

About 2.2 million people in the U.S. have Glaucoma. POAG is often associated with increased eye pressure but about one-third of patients have normal pressure Glaucoma (NPG). Currently, no curative treatments exist for NPG.
Researchers including lead author Janey Wiggs, M.D., Ph.D., and Lou Pasquale, M.D., Co-Directors of the Harvard Glaucoma Center of Excellence, analyzed DNA sequences of 6,633 participants, half of whom had POAG. Participants were part of two NIH-funded studies: GLAUGEN (Glaucoma Genes and Environment) and NEIGHBOR (NEI Glaucoma Human genetics collaBORation), conducted at 12 sites in the United States. Dr. Pasquale is Director of the Glaucoma Service at Mass. Eye and Ear.
The results, reported online in PLoS Genetics (April 26, 2012), found that two variations were associated with POAG, including NPG. These are the first variants commonly associated with NPG. One variant is in a gene located on chromosome 9 called CDKN2BAS whereas the other variant is in a region of chromosome 8 where it may affect the expression of genes LRP12 or ZFPM2. These genes may interact with transforming growth factor beta (TGF-beta), a molecule that regulates cell growth and survival throughout the body. Previous studies have also implicated TGF-beta in Glaucoma.
"This research has provided important new insights into the disease pathogenesis and will make future studies focused on translating this information into the clinic possible. Ultimately we hope to prevent blindness caused by this very common eye disease," said lead author Dr. Wiggs.
"This study has identified an important molecular pathway in the development of POAG. Control of TGF-beta might lead to more effective therapies for this blinding disease," said Dr. Hemin Chin, associate director for Ophthalmic Genetics at the National Eye Institute.
Funding sources for this research include the National Eye Institute, National Human Genome Research Institute, Lions Eye Research Fund, Glaucoma Center of Excellence, the Margolis Fund, and Research To Prevent Blindness.
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Future Treatment for Nearsightedness - Compact Fluorescent Light Bulbs?

Future Treatment for Nearsightedness - Compact Fluorescent Light Bulbs?

ScienceDaily (May 8, 2012) - Researchers at the University of Alabama at Birmingham hope to one day use fluorescent light bulbs to slow Nearsightedness, which affects 40 percent of American adults and can cause blindness.

In an early step in that direction, results of a study found that small increases in daily artificial light slowed the development of Nearsightedness by 40 percent in tree shrews, which are close relatives of primates.
The team, led by Thomas Norton, Ph.D., professor in the UAB Department of Vision Sciences, presented the study results May 8 at the 2012 Association for Research in Vision and Ophthalmology annual meeting in Ft. Lauderdale.
People can see clearly because the front part of the eye bends light and focuses it on the retina in back. Nearsightedness, also called myopia, occurs when the physical length of the eye is too long, causing light to focus in front of the retina and blurring images.
Myopia has many causes, some related to inheritance and some to the environment. Research in recent years had, for instance, suggested that children who spent more time outdoors, presumably in brighter outdoor light, had less myopia as young adults. That raised the question of whether artificial light, like sunlight, could help reduce myopia development, without the risks of prolonged sun exposure, such as skin cancer and cataracts.
"Our hope is to develop programs that reduce the rate of myopia using energy efficient, fluorescent lights for a few hours each day in homes or classrooms," said John Siegwart, Ph.D., research assistant professor in UAB Vision Sciences and co-author of the study. "Trying to prevent myopia by fixing defective genes through gene therapy or using a drug is a multi-year, multimillion-dollar effort with no guarantee of success. We hope to make a difference just with light bulbs."
Sorting through theories
Work over 25 years had shown that putting a goggle over one eye of a study animal, one that lets in light but blurs images, causes the eye to grow too long, which in turn causes myopia. Other past studies had shown that elevated light levels could reduce myopia under these conditions, whether the light was produced by halogen lamps, metal halide bulbs or daylight. The current study is the first to show that the development of myopia can be slowed by increasing daily fluorescent light levels.
One prevailing theory on myopia-related shape changes in the eye is that they are caused by the blurriness of images experienced while reading or doing other near-work chores. Another holds some people develop myopia because they have low levels of vitamin D, which goes up with exposure to sunlight and could explain the connection between outdoor light and reduced myopia. A third theory, one reinforced by the current results, is that bright light causes an increase in levels of dopamine, a signaling molecule in the retina.
To test the theories, the team used a goggle that lets in light but no images to produce myopia in one eye of each tree shrew. They found that a group exposed to elevated fluorescent light levels for eight hours per day developed 47 percent less myopia than a control group exposed to normal indoor lighting, even though the images were neither more nor less blurry. They also found that animals fed vitamin D supplements developed myopia just like ones without the supplement. Given these results, the team is now experimenting with light levels and treatment times to see if a short, bright light treatment could be effective. They have also begun studies looking at the effect of elevated light on retinal dopamine levels as it relates to the reduction of myopia.
"If we can find the best kind of light, treatment period and light level, we'll have the scientific justification to begin studies raising light levels in schools, for instance," said Norton. "Compact fluorescent bulbs use much less electricity than standard light bulbs, and future programs raising light levels will have more impact the less expensive they are."
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DHA, prevented age-related vision loss

An omega-3 fatty acid found in fish, known as DHA, prevented age-related vision loss in lab tests, according to recent medical research from the University of Alberta.

Yves Sauvé, a researcher in the Faculty of Medicine & Dentistry, and his team discovered that lab models fed DHA did not accumulate a toxic molecule at the back of the eyes. The toxin normally builds up in the retina with age and causes vision loss.

"This discovery could result in a very broad therapeutic use," says Sauvé, whose work was recently published in the peer-reviewed journalInvestigative Ophthalmology & Visual Science.

"In normal aging, this toxin increases twofold as we age. But in lab tests, there was no increase in this toxin whatsoever. This has never been demonstrated before -- that supplementing the diet with DHA could make this kind of difference."

The team recently started another study, looking at people who have age-related macular degeneration, a condition that results in loss of central vision and is the main cause of blindness in people over the age of 50. The researchers will look for DNA markers in the blood of study participants. The team wants to determine whether participants with certain genetic markers will respond better to increasing amounts of DHA in their diet, and if so, why.

Sauvé is a researcher in the departments of ophthalmology and physiology at the U of A.

Various organizations funded the research; the primary funder was the Canadian Institutes of Health Research.

ScienceDaily (May 30, 2012) — 

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The above story is reprinted from materials provided byUniversity of Alberta Faculty of Medicine & Dentistry. The original article was written by Raquel Maurier.

Positive Stress’ Helps Protect Eye from Glaucoma

Positive Stress’ Helps Protect Eye from Glaucoma


ScienceDaily (Apr. 3, 2012) — Working in mice, scientists at Washington University School of Medicine in St. Louis have devised a treatment that prevents the optic nerve injury that occurs in Glaucoma, a neurodegenerative disease that is a leading cause of blindness.

Researchers increased the resistance of optic nerve cells to damage by repeatedly exposing the mice to low levels of oxygen similar to those found at high altitudes. The stress of the intermittent low-oxygen environment induces a protective response called tolerance that makes nerve cells -- including those in the Eye -- less vulnerable to harm.

The study, published online inMolecular Medicine, is the first to show that tolerance induced by preconditioning can protect against a neurodegenerative disease.

Stress is typically thought of as a negative phenomenon, but senior author Jeffrey M. Gidday, PhD, associate professor of neurological surgery and ophthalmology, and others have previously shown that the right kinds of stress, such as exercise and low-oxygen environments, can precondition cells and induce changes that make them more resistant to injury and disease.

Scientists previously thought tolerance in the central nervous system only lasted for a few days. But last year Gidday developed a preconditioning protocol​ that extended the effects of tolerance from days to months. By exposing mice to hypoxia, or low oxygen concentrations, several times over a two-week period, Gidday and colleagues triggered an extended period of tolerance. After preconditioning ended, the brain was protected from stroke damage for at least 8 weeks.

"Once we discovered tolerance could be extended, we wondered whether this protracted period of injury resistance could also protect against the slow, progressive loss of neurons that characterizes neurodegenerative diseases," Gidday says.

To find out, Gidday turned to an animal model of Glaucoma, a condition linked to increases in the pressure of the fluid that fills the Eye. The only treatments for Glaucoma are drugs that reduce this pressure; there are no therapies designed to protect the retina and optic nerves from harm.

Scientists classify Glaucoma as a neurodegenerative disease based on how slowly and progressively it kills retinal ganglion cells. The bodies of these cells are located in the retina of the Eye; their branches or axons come together in bundles and form the optic nerves. Scientists don't know if damage begins in the bodies or axons of the cells, but as more and more retinal ganglion cells die, patients experience peripheral vision loss and eventually become blind.

For the new study, Yanli Zhu, MD, research instructor in neurosurgery, induced Glaucoma in mice by tying off vessels that normally allow fluid to drain from the Eye. This causes pressure in the Eye to increase. Zhu then assessed how many cell bodies and axons of retinal ganglion cells were intact after three or 10 weeks.

The investigators found that normal mice lost an average of 30 percent of their retinal ganglion cell bodies after 10 weeks of Glaucoma. But mice that received the preconditioning before Glaucoma-inducing surgery lost only 3 percent of retinal ganglion cell bodies.

"We also showed that preconditioned mice lost significantly fewer retinal ganglion cell axons," Zhu says.

Gidday is currently investigating which genes are activated or repressed by preconditioning. He hopes to identify the changes in gene activity that make cells resistant to damage.

"Previous research has shown that there are literally hundreds of survival genes built into our DNA that are normally inactive," Gidday says. "When these genes are activated, the proteins they encode can make cells much less vulnerable to a variety of injuries."

Identifying specific survival genes should help scientists develop drugs that can activate them, according to Gidday.

Neurologists are currently conducting clinical trials to see if stress-induced tolerance can reduce brain damage after acute injuries like stroke, subarachnoid hemorrhage or trauma.

Gidday hopes his new finding will promote studies of tolerance's potential usefulness in animal models of Parkinson's disease, Alzheimer's disease and other neurodegenerative conditions.

"Neurons in the central nervous system appear to be hard-wired for survival," Gidday says. "This is one of the first steps in establishing a framework for how we can take advantage of that metaphorical wiring and use positive stress to help treat a variety of neurological diseases."