A Review of Age-Related Macular Degeneration
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Age related macular degeneration (AMD) is one of the first prospective targets for prototype rejuvenation treatments. This is because the relationship between the condition and one of the primary forms of change between young and old tissue is both direct and comparatively well understood: certain hardy metabolic waste compounds accumulate in long-lived retinal cells to cause increasing dysfunction over the timescale of a human life span, and this occurs because our cellular recycling machinery cannot effectively break down these compounds. The best solution is to develop drugs or make use of tools such as bacterial enzymes that can do this for us; comparatively few groups are working on this angle, however.

Ageing disorders can be defined as the progressive and cumulative outcome of several defective cellular mechanisms as well as metabolic pathways, consequently resulting in degeneration. Environment plays an important role in its pathogenesis. Age related macular degeneration (AMD) is one such retinal degenerative disorder which starts with the progression of age. Metabolism plays an important role in initiation of such diseases of ageing. Cholesterol metabolism and their oxidized products like 7-ketocholesterol have been shown to adversely impact retinal pigment epithelium (RPE) cells. These molecules can initiate mitochondrial apoptotic processes and also influence the complements factors and expression of angiogenic proteins like VEGF etc.

Age related macular degeneration (AMD) is described by irreversible vision loss in older age. The disease pathology emerges with the degeneration of macula which forms the central part of retina. The macula consists of photoreceptor (rods and cones) important for central vision. As AMD symptoms appear, characteristic features such as formation of drusen, consisting of active and inactive complement associated inflammatory products, aggregate of lipoprotein, cell debris, oxysterols, oxidized phospholipids and Alu RNA deposits begin to emerge later in life.

These aggregates deposit in the extra-cellular space between Bruch's membrane and retinal pigment epithelium cells (RPE). Gradual and consistent effects of these aggregates gradually cause degeneration of these cells followed by global atrophy of RPE cells, commonly known as geographic atrophy (GA). Besides, active inflammatory components of these deposits between Bruch's membrane and RPE, stimulate angiogenic factors (e.g., VEGF, TGFB etc.) which act on choriocapillary network beneath the Bruch's membrane and stimulate proliferation to new blood vessels (a process called neovascularization). These newly formed blood vessels can outgrow into the RPE cells and result in disruption of RPE cell integrity and function which is well preserved in early life.

Link: http://journal.frontiersin.org/Journal/10.3389/fnagi.2014.00151/full

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