Richismita Hazra, Amity University Kolkata
Macular degeneration is an eye disease that causes loss in the centre of the field of vision and often leads to irreversible blindness. The disease is broad of two types: dry macular degeneration in which there is a deterioration of the centre of the retina and wet macular degeneration that leads to the growth of leaky blood vessels under the retina. This study deals with a third kind, known as age-related macular degeneration (AMD), in which the central high-resolution vision is destroyed in more than 30 million older adults over 60 years of age. AMD remains to be a major medical as well as socioeconomic challenge globally and due to the growing ageing population with elevated life expectancies, the number of AMD cases is expected to be doubled by 2025. The lack of effective therapies for the disease may cause impaired vision in more than 2800 million people by the year 2040.
Cholesterol, a fatty acid, is an important fuel source for the retina that is taken up by photoreceptors for maintaining metabolic demands of the eye. Retinal pigment epithelium (RPE), a polarized monolayer of post-mitotic cells that resides in the outer retina is the chief site of injury in AMD. In AMD, macrophages are unable to maintain intracellular homeostasis which results in the accumulation of oxidized fatty acids. This in turn activates various signalling pathways leading to macrophage malfunctioning thereby causing deposits and drusen. So AMP is vigorously associated with heterogeneity in genes that control complement activation and cholesterol metabolism.
Though many newer facts have been uncovered about AMD, the biology underlying disease-associated variants are not yet well understood. Recently researchers have used molecular, biochemical and live-cell imaging methods to shed light on mechanisms by which ageing-associated insults intrigue with AMD genetic risk variants. This study showed how RPE had to trade-offs major and critical functions like lipid metabolism, autophagy, compliment regulation and mitochondrial dynamics. This led way to a deeper understanding of these mechanisms and identification of the promising therapeutic targets for the preservation of RPE homeostasis in AMD.
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Source: Department of Ophthalmology, School of Medicine, University of California, San Francisco, CA, USA Pharmaceutical Sciences and Pharmacogenomics Graduate Program, University of California, San Francisco, CA, USA Department of Anatomy, School of Medicine, University of California, San Francisco, CA, USAhttps://doi.org/10.1016/j.redox.2020.101781
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