He is an ophthalmologists, professor of clinical ophthalmology, chief of glaucoma services at the New York Eye and Ear Infirmary, and medical director and chairman of the scientific advisory board of the Glaucoma Foundation.

Robert Ritch, MD

home

authors

robert-ritch-md

In a small study, a combination over-the-counter supplement with antioxidant and mitoprotective properties significantly reversed mitochondrial dysfunction.

A supplement with antioxidant and mitoprotective properties reversed mitochondrial dysfunction and may be neuroprotective in glaucoma, according to study results presented by Robert Ritch, MD, Steven and Shelley Einhorn Distinguished Chair and Professor of Ophthalmology at New York Eye and Ear Infirmary of Mount Sinai, New York.

Dr. Ritch and co-investigators from Ramathibodi Hospital, Mahidol University, Bangkok, Thailand, and Columbia University, New York, presented a poster with their findings at the American Glaucoma Society meeting in New York earlier this year.

The study focused on whether a combination of over-the-counter supplements with antioxidant and mitoprotective properties could reverse mitochondrial dysfunction by reducing mitochondrial flavoprotein fluorescence compared with placebo.

A total of 14 patients (n = 28 eyes) were divided into either a placebo group or a group that received a combination of curcumin, Ginkgo biloba extract, citicoline, coenzyme-Q10 (upiquinol, Cognizin), N-acetyl-cysteine, alpha-lipoic acid, grapeseed extract, and green tea extract. All of the aforementioned are part of a supplement called GlaucoHealth.

The study was performed as part of an investigational new drug application from the FDA.

Visual fields, optical coherence tomography (OCT), and retinal metabolic analysis were performed at baseline and at 1 and 3 months after randomization.

Researchers monitored for changes in visual fields, OCT, and retinal metabolic analysis over time. The initial demographic characteristics of the two groups were similar.

There were no significant differences in visual field or OCT indices in either group (all p > 5%).

However, there was a significant decrease in optic nerve adjusted mitochondrial flavoprotein fluorescence and average curve width from baseline to 1 month in those treated with GlaucoHealth (` = –39, p = 0.003; ` = –0.25, p = 0.01, respectively) but not in patients who were treated with placebo (p = 0.47 and 0.23).

“Mitochondrial dysfunction and death are increasingly implicated in retinal ganglion cell death in glaucoma and neuronal death in other neurodegenerative disorders,” Dr. Ritch said. “Mitochondria become dysfunctional and die prior to neuronal cell death.

“Formulations with IOP-dependent neuroprotective effects could be additive in slowing progression rates by reversing mitochondrial dysfunction,” he said.

Research such as that from this study could shift the treatment paradigm to stabilize mitochondria at an earlier disease stage, and prevent or retard neuronal cell death, the poster explained.

The findings “serve as a proof-of-concept for future trials testing the neuroprotective effect of supplement combinations in glaucoma,” according to the poster.

This article was adapted from a poster presentation at the 2018 meeting of the American Glaucoma Society in New York earlier this year. The authors did not indicate any proprietary interest relevant to the subject matter.

Articles

Antioxidant, mitoprotective duo reverses mitochondrial dysfunction

A patient with glaucoma and XFS has higher IOP, worse optic disc and field damage, and a greater failure rate with medical therapy than individuals with primary open-angle glaucoma, said Dr. Ritch, surgeon director and chief of glaucoma services at The New York Eye and Ear Infirmary, New York, professor of clinical ophthalmology at New York Medical College, Valhalla, and one of the chairmen of the meeting. 

Studies have shown that the risk of development of glaucoma in those with ocular hypertension and the risk of progression of glaucomatous damage for patients with XFS with glaucoma is double that of those without the condition, Dr. Ritch said. 

Predisposing factors for angle-closure associated with XFS include zonular weakness (a thicker lens and anterior lens movement), rigidity of the iris, a sluggish pupil, and posterior synechiae. Cataract is also associated with the syndrome. Unilateral cataract and XFS are almost invariably in the same eye, with ischemia or oxidative damage possible causes. 

When it comes to cataract surgery, the complication rate for such patients is 7 to 10 times greater with extracapsular cataract extraction, less with phacoemulsification. Predisposing factors such as posterior synechiae, zonular weakness, fragility of the capsule, phacodonesis, and poor pupillary dilation lead to complications that include zonular dehiscence, capsular rupture, and loss of vitreous. 

XFS appears to be associated etiologically with retinal vein occlusion. In addition, XFS is a systemic disease, Dr. Ritch emphasized. Exfoliation-like fibrils can be found in many organs-the heart, lung, meninges, kidney, skin, liver, gall bladder, and blood vessels. It is associated with transient ischemic attacks, stroke, angina, myocardial infarctions, Alzheimer's disease, and hearing loss. Reported ocular blood flow abnormalities include reduced ipsilateral and pulsatile ocular blood flow, reduced flow to the optic nerve head and peripapillary retina, and an increased incidence of disc hemorrhage. 

XFS appears to be a member of the family of conformational disorders, which arise from an abnormal arrangement of proteins that results in a harmful gain or loss of biological function, Dr. Ritch explained. Other conformational diseases include Alzheimer's disease, Parkinson's disease, Huntington's disease, cystic fibrosis, and type II diabetes, he said. 

There are suggestions that XFS could have an infectious origin, Dr. Ritch said. There are reports of younger patients developing the condition after receiving corneal transplants from elderly donors. One suspect is herpes simplex, he said, citing a study that found the virus in the iris and anterior capsules of 13.9% of 64 eyes from patients with XFS but only 1.75% of 61 eyes from persons without the condition. 

But there is "still insufficient evidence to suggest a causal relationship between any specific infectious agent and XFS," he said. 

Whatever its cause, "non-IOP-lowering treatment modalities are potentially applicable to XFS," Dr. Ritch said. 

And if the cause is identified, "we are looking at what is potentially a curable disease," he added. 

Glaucoma 2006 was sponsored by The New York Eye and Ear Infirmary, the UMDNJ-Center for Continuing & Outreach Education, the New York Society for Clinical Ophthalmology, The Academy of Healthcare Education Inc., and CME

 , an independent subsidiary of Advanstar Communications Inc., publisher of 

. Pfizer Inc. provided an unrestricted educational grant for the program. 

New York-A patient with exfoliation syndrome (XFS) may have the worst type of open-angle glaucoma, according to Robert Ritch, MD, who opened a session on XFS at the Glaucoma 2006 meeting.

Robert Ritch, MD

Articles

Antioxidant, mitoprotective duo reverses mitochondrial dysfunction

XFS puts individuals at great risk for blindness

New content coming soon, please check back later.