Retinal Inflammaging: Pathogenesis and Prevention
Abstract
Macula lutea, the yellow sot or fovea centralis in eye serves the distinctive central vision in perceiving visual cues and contributing to task performance. Impaired visual acuity in later years in life, compromises safety, productivity and life quality. Carotenoid pigment content declines with cumulation of light induced damage through aging process in retina. The progression of resultant macular degeneration is aggravated by oxidative stress, inflammation, raised blood sugar and vasculopathy associating aging. Senescent dry degeneration involves drusen (a compound of glycolipid and glycol-conjugate core) deposition that impairs metabolic connectivity of upper layers of retina with choroid. Degeneration of retinal pigment epithelium (RPE) and photoreceptors thus, results. The late more severe form of age related macular degeneration (AMD), involves factors inducing choroidal neo-vascularization. Leaky neo-capillaries speed degenerative process of retina. Most age related pathologies are initiated by metabolic disruptions and AMD shares features of systemic atherosclerosis. An aberrant tissue response to free radical stress, vasculopathy and local ischaemic underlies AMD pathogenesis.
There is no specific treatment modality and prudent strategy in prophylaxis only. Early diagnosis and proper control of environmental and lifestyle factors are strived by newer biomedical understanding, which is briefly reviewed.| PDF |
References
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