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Home ยป Aging of the Eye Can Accelerate With Repeated Stress
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Aging of the Eye Can Accelerate With Repeated Stress

BryarBy BryarJanuary 14, 2023No Comments4 Mins Read
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Credit: Josh Sorenson/ Pexels
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Stress causes retinal aging to create symptoms much like those that naturally occur with aging.

Age plays a significant role in the death of retinal ganglion cells in glaucoma, and new treatment methods for glaucoma patients might target these pathways, according to research from the University of California, Irvine.

The study was published in Aging Cell and was carried out by Dorota Skowronska-Krawczyk, Ph.D., and her co-authors. The study looks at the epigenetic and transcriptional changes which take place in the aging retina and how stress and anxiety can result in the retina to undergo similar modifications to natural aging. Additionally, the study suggests that repeated pressure in the young retinal tissue could speed up aging.

The process of aging is common and impacts all cells in a body. It is a significant risk factor for glaucoma, a group of neuropathies referred to as a group in the eye. Due to the increase in aging populations worldwide, current estimates show that the number of individuals with glaucoma (aged 40-80) increases to over 110 million in 2040.

When the UCI-led team investigated the optic nerve head of eyes treated with mild pressure elevation, they noted that in the young optic nerve head, there was no sign of loss of axons. However, in the optic nerves of old animals, significant sectorial loss of axons was observed similar to the phenotype commonly observed in glaucoma patients. Credit: UCI School of Medicine

“Our work emphasizes the significance of earlier diagnosis and prevention in addition to age -specific management of age related diseases including glaucoma,” Skowronska-Krawczyk said. The epigenetic modifications that we observed suggest that changes at chromatin level are acquired after a number of instances of stress in an cumulative way. This opens up a window of possibility for the defense against vision loss if and when the condition is recognized early on. “

IOP has a circadian rhythm in humans. In healthy individuals it oscillates ordinarily in the 12-21 mmHg range, and also is likely to be highest in the nocturnal period in approximately two-thirds of individuals. A single measurement of IOP is often insufficient to characterize the true pathology along with the chance of disease progression in glaucoma individuals due to IOP fluctuations. The long-term variation of IOP was reported as a good predictor of glaucoma development. This study indicates the cumulative effect of variations in IOP is directly accountable for the getting old of the tissue.

“even moderate hydrostatic IOP elevation leads to retinal ganglion cell damage and associated visual defects in more mature animals,” Skowronska-Krawczyk said. “We are continuing to work to recognize the mechanism of cumulative variations in aging, to look for potential targets for therapeutics,” she said. We are also testing different strategies to avoid the accelerated aging process that results from stress. “

This work renders possible a new tool that enables researchers to estimate the effect of treatment and stress on the aging state of retinal tissue. In collaboration with the Clock Foundation and Steve Horvath, Ph.D., from Altos Labs, scientists were able to demonstrate that repetitive, mild IOP elevations are able to accelerate the epigenetic age of tissues.

“In addition to evaluating vision drop and some structural changes as a result of stress and potential treatment, we can now evaluate the epigenetic era of retinal tissue, and use it to find the best strategy to prevent vision loss in aging,” Skowronska Krawczyk said.

The research was supported by the National Institutes of Health, the Foundation for The European and polish Science Union under the European Regional Development Fund. The authors thank the Research to prevent Blindness Foundation for their support of the Department of Ophthalmology at UCI.

DOI: 10.1111/acel.13737

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