January Is National Glaucoma Awareness Month

January is National Glaucoma Awareness Month, an important time to spread the word about this sight-stealing disease. Currently, more than three million people in the United States have glaucoma. The National Eye Institute projects this number will reach 4.2 million by 2030, a 58 percent increase. Glaucoma is called "the sneak thief of sight" since there are no symptoms and once vision is lost, it's permanent. As much as 40 percent of vision can be lost without a person noticing.

Glaucoma is the leading cause of irreversible blindness. Moreover, among African American and Latino populations, glaucoma is more prevalent. Glaucoma is six to eight times more common in African Americans than Caucasians. Over three million Americans, and over 60 million people worldwide, have glaucoma. Experts estimate that half of them don't know they have it. Combined with our aging population, we can see an epidemic of blindness looming if we don't raise awareness about the importance of regular eye examinations to preserve vision. The World Health Organization estimates that 4.5 million people worldwide are blind due to glaucoma.

Help Raise Awareness

Talk to your family about glaucoma. In the United States, approximately 120,000 are blind from glaucoma, accounting for nine percent to 12 percent of all cases of blindness. Here are three ways you can help raise awareness:

  1. Talk to friends and family about glaucoma. If you have glaucoma, don’t keep it a secret. Let your family members know.
  2. Refer a friend to the Glaucoma Research Foundation web site, glaucoma.org.
  3. Request to have a free educational bookletsent to you or a friend.
  4. Get involved in your communitythrough fundraisers, information sessions, group discussions, inviting expert speakers, and more.
  5. Share information about glaucoma with your friends and family.

What is Glaucoma?

Glaucoma is a group of eye diseases that gradually steal sight without warning. Although the most common forms primarily affect the middle-aged and the elderly, glaucoma can affect people of all ages. Vision loss is caused by damage to the optic nerve. This nerve acts like an electric cable with over a million wires. It is responsible for carrying images from the eye to the brain. There is no cure for glaucoma - yet. However, medication or surgery can slow or prevent further vision loss. The appropriate treatment depends upon the type of glaucoma among other factors. Early detection is vital to stopping the progress of the disease.

Types Of Glaucoma

There are two main types of glaucoma: primary open-angle glaucoma (POAG), and angle-closure glaucoma. These are marked by an increase of intraocular pressure (IOP), or pressure inside the eye. When optic nerve damage has occurred despite a normal IOP, this is called normal tension glaucoma. Secondary glaucoma refers to any case in which another disease causes or contributes to increased eye pressure, resulting in optic nerve damage and vision loss.

In the most common form, there are virtually no symptoms. Vision loss begins with peripheral or side vision, so if you have glaucoma, you may not notice anything until significant vision is lost. The best way to protect your sight from glaucoma is to get a comprehensive eye examination. Then, if you have glaucoma, treatment can begin immediately.

Will CBD Worsen Glaucoma?

One of the most commonly proposed uses of medical marijuana is to treat glaucoma. But a study - in the journal Investigative Ophthalmology & Visual Science - from researchers at Indiana University has found that a major chemical component in the substance appears to worsen the primary underpinning of the disease: a rise in pressure inside the eye. The chemical that causes this rise in pressure is cannabidiol, or CBD, a non-psychoactive ingredient in cannabis that is increasingly marketed to consumers in products such as oil, gummies, creams and health food.

It is also approved in many states as a treatment for conditions such as pediatric epilepsy. "This study raises important questions about the relationship between the primary ingredients in cannabis and their effect on the eye," said Alex Straiker, an associate scientist in the IU Bloomington College of Arts and Sciences' Department of Psychological and Brain Sciences, who led the study. "It also suggests the need to understand more about the potential undesirable side effects of CBD, especially due to its use in children."

The study, which was conducted in mice, specifically found that CBD caused an increase in pressure inside the eye of 18 percent for at least four hours after use. Tetrahydrocannabinol, or THC, the primary psychoactive ingredient of marijuana, was found to effectively lower pressure in the eye, as has been previously reported. But the study found that the use of CBD in combination with THC blocked this effect. Specifically, the study found that male mice experienced a drop in eye pressure of nearly 30 percent eight hours after exposure to THC alone. A lower pressure drop of 22 percent was also observed after four hours in male mice.

The effect was weaker in female mice. This group experienced a pressure drop of only 17 percent after four hours. No difference in eye pressure was measured after eight hours. The results suggest that females may be less affected by THC, though it isn’t clear whether this extends to the substance's psychoactive effects. "This difference between males and females and the fact that CBD seems to worsen eye pressure, the primary risk factor for glaucoma, are both important aspects of this study," Straiker says. "It’s also notable that CBD appears to actively oppose the beneficial effects of THC."

By comparing the effect of these substances on mice without specific neuroreceptors affected by THC and CBD, the IU researchers were also able to identify the two specific neuroreceptors - named CB1 and GPR18 - by which the first substance lowered pressure inside the eye. "There were studies over 45 years ago that found evidence that THC lowers pressure inside the eye, but no one's ever identified the specific neuroreceptors involved in the process until this study," Straiker said. "These results could have important implications for future research on the use of cannabis as a therapy for intraocular pressure."

Treatment To Stop Glaucoma

Vision scientists at the University of California, Berkeley, and the University of Toronto have discovered that naturally occurring molecules known as lipid mediators have the potential to halt the progression of glaucoma. Their findings - published in the Journal of Clinical Investigation - mark a major step forward in the pursuit of a cure for glaucoma. "Not only could this discovery lead to drugs to treat glaucoma, but the same mechanism, and options for prevention, may be applicable to other neurodegenerative diseases," says study senior author Karsten Gronert, professor of optometry and chair of vision science at UC Berkeley.

Using rodent models, Gronert and fellow researchers found that inflammation-regulating lipid mediators known as lipoxins, secreted from star-shaped cells known as astrocytes, stopped the degeneration of retinal ganglion cells in rats and mice with glaucoma. Ganglion cells are the neurons of the retina and optic nerve that receive information from photoreceptors. "We've taken something everyone assumed was anti-inflammatory, and found that these same small molecules play a key role in neuroprotection, which is really exciting," says study co-senior author John Flanagan, dean and professor of optometry.

Specifically, researchers found that astrocytes, which help maintain brain function and form the nerve fiber layer of the retina and optic nerve, release therapeutic biological agents known as lipoxins A4 and B4, but only when the astrocytes are at rest and maintaining nerve function. "It is commonly assumed that astrocytes activated by injuries release stress signals that kill off ganglion cells in the retina, causing optic nerve damage," said Flanagan. "However, our research discovered that astrocytes that are triggered by injury actually turn off novel neuroprotective signals that prevent optic nerve damage."

Reversing Cell Death

Researchers discovered secretions of lipoxins A4 and B4 in resting astrocytes in culture in the retina and optic nerve head. To test their potential as a treatment, they administered the lipoxins to rodents eight weeks after the onset of glaucoma-like damage and neurodegeneration. At 16 weeks, they gauged electrical activity in the rodents' ganglion cells, among other measures, and found that lipoxin B4 in particular stopped the cells' degeneration. "This little-known lipid mediator has shown the potential to reverse cell death," Gronert said. "We know of no drug that can do this."

For decades, pharmaceutical companies have searched for neuroprotective drugs to treat glaucoma and other disorders marked by the death of nerve cells such as Alzheimer's, Parkinson's and ALS. Glaucoma is by far the most prevalent of these neurodegenerative diseases. "At the same time, lipoxins have been explored as promising drug targets for treating inflammatory diseases, but nobody has been looking at them as being neuroprotective," Gronert said. At present, the treatment option for glaucoma is to lower ocular pressure, but there are no effective treatments for preventing or stopping the neurodegeneration of glaucoma, which is irreversible and eventually leads to blindness, Flanagan said

The study authors are excited at the prospect of further investigations into the therapeutic benefits and mechanisms of lipoxins A4 and B4 and their potential to stop or reverse neural damage. They have jointly filed a patent application for use of lipoxin A4 and B4 to treat glaucoma and neurodegenerative diseases. Their eventual goal is to test the lipoxins as drugs in humans. "These naturally occurring small lipids have great potential as therapies because they may play a fundamental role in preventing other neurodegenerative diseases. And that's hugely significant," Flanagan said.

Glaucoma Risk

Researchers at the Center for Vascular Research, within the Institute for Basic Science (IBS), have identified a new mechanism involved in the development and progression of glaucoma, and found a potential therapeutic option to treat it. This study - published in the Journal of Clinical Investigation - is expected to help the development of therapies to treat primary open-angle glaucoma (POAG), which counts for three quarters of all glaucoma patients.

One of the most important risk factors for glaucoma is the increased pressure inside the eye. A liquid called aqueous humor is constantly produced and drained out from the eye. It transports nutrients and inflates the eye giving it a roughly spherical shape. However, if this fluid cannot flow out of the eye chambers freely, an increase in intraocular pressure can damage the optic nerve, leading to vision loss. The precise mechanism of elevated resistance to aqueous humor outflow remains unclear, and although the current treatments for glaucoma tackle the production and outflow of aqueous humor, their outcomes are still poor.

A component of the eye that plays a fundamental role in draining out the aqueous humor is Schlemm's canal. It collects the aqueous humor and mediates its transfer from the eye chambers to blood circulation. The cells on the walls of the canal, endothelial cells, ship the liquid from the inner to the outer side in "packages," called vacuoles. As the shape and number of the vacuoles reflects the outflow performance, several giant vacuoles are expected in the normal outflow process.

The IBS team explained how imbalances in Schlemm's canal significantly increase the risk of glaucoma. They showed that an important regulator for canal functionality is the angiopoietin-Tie2 system. Angiopoietins, such as Ang1 and Ang2, are proteins important for the growth of new blood vessels and Tie2 is the receptor that binds them. It is known that the angiopoietin-Tie2 system plays a role in Schlemm's canal formation, as Tie2 mutations or angiopoietin absence result in congenital glaucoma. However, this study clarified that it is also critically important during adulthood.

Therapeutics Development

The researchers reported that adult mice deficient in Tie2 suffer from an elevated intraocular pressure, retinal neuronal damage and partial visual impairment. Moreover, they had a markedly decreased number of giant vacuoles inside Schlemm's canal endothelial cells, which indicate a poor aqueous humor drainage. The scientists also investigated if and how this process changes in older mice, as aging is a major risk factor for glaucoma, and showed that aged mice experience reduced levels of giant vacuoles, Tie2, Ang1, and Ang2, as well as other proteins connected with the angiopoietin-Tie2 pathway, like Prox1.

To test whether Tie2 activation could shift the situation, the researchers tested the antibody ABTAA - Ang2-binding and Tie2-activating antibody. They injected it in one eye of mice, while the other eye of the same mice functioned as the negative control. After one week, levels of Tie2 and Prox1, number and diameter of giant vacuoles in Schlemm's canals increased in the ABTAA-treated eyes compared to control eyes.

The researchers observed a similar outcome with decreased intraocular pressure when ABTAA was injected to the eyes of mice suffering from POAG with regressed Schlemm's canals, indicating that this antibody might be considered as a therapeutic option. "Slow development of glaucoma treatments is partly due to the poor understanding of the underlying pathogenesis," says KOH Gou Young, the corresponding author of the study. "We hope that identifying the critical role of the angiopoietin-Tie2 system in adult Schlemm's canals will bring a significant boost in the development of therapeutics."

Good Glaucoma News

There is a misconception that glaucoma is untreatable and will inevitably cause blindness. But, Dr. Andrea Zimmerman, a low vision specialist at Lighthouse Guild says, “There are new medications and procedures to treat glaucoma. In addition, there are promising studies underway. One of these involves developing an implant that could be inserted surgically to dispense medication,” she says. This is good news for those who have been diagnosed and those who are at risk. She points out that getting regular eye exams is the first step in protecting your eyes from glaucoma and other eye disorders that can lead to vision loss. A comprehensive dilated eye exam can detect glaucoma in its early stages allowing you to get treatments that can prevent loss of vision. “Early intervention is the key to preventing vision loss,” Dr. Zimmerman says. “Regular eye exams should start by age 3. Although it is rare, even children can have glaucoma.” 

Many people experience difficulty with vision as they get older. Problems with reading, driving at night, glare, peripheral vision, and walking due to the inability to see curbs and steps, can be common. “It’s important not to ignore these problems,” says Dr. Zimmerman. “You need to get them checked out. Only an eye care professional can determine if these symptoms are related to glaucoma or other eye conditions and begin treatments that can help safeguard your vision.” For those who do have vision loss from glaucoma, studies have found that vision rehabilitation can improve quality of life and the ability to perform daily tasks. Dr. Zimmerman says, “At Lighthouse Guild, we provide vision rehabilitation and other services to help people who have vision loss due to glaucoma, or other causes, lead full and productive lives.”

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