IRP researchers discover potential therapeutic target for degenerative eye disease

Study reveals cellular pathology of 'dry' AMD

Researchers from the National Institutes of Health (NIH) have discovered the source of dysfunction in the process whereby cells in the eye's retina remove waste.

A report by scientists at NIH and Johns Hopkins University, Baltimore, details how alterations in a factor called AKT2 affects the function of organelles called lysosomes and results in the production of deposits in the retina called drusen, a hallmark sign of dry age-related macular degeneration (AMD). According to the researchers, the findings suggest drusen formation is a downstream effect of AKT2-related lysosome dysfunction and points to a new target for therapeutic intervention.

Lysosomes are like cells' garbage disposals, and they play a crucial role in maintaining the eye's light-sensing retina. Key cells that make up the retinal pigment epithelium (RPE) provide oxygen and nutrients to the retina's energetically active neurons. They also collect and processes the retina’s waste products through lysosomes. Failure in the cells’ ability to process these waste products leads to the formation of drusen. As AMD progresses, drusen increase in number and volume. But despite intensive research, drusen formation is still largely a mystery.

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This page was last updated on Friday, July 26, 2024