AMYLOID-β RISK FACTOR FOR AGE-RELATED MACULAR DEGENERATION

• Published in: Innovation in aging Vol. 1; no. suppl_1; pp. 427 - 428
• Main Authors: Bobrov, A.P., Ermilov, V.V., Smirnov, A.
• Format: Journal Article
• Language: English
• Published: US Oxford University Press 01.07.2017
• Subjects: Abstracts
• ISSN: 2399-5300; 2399-5300
• DOI: 10.1093/geroni/igx004.1536

Age-related macular degeneration (AMD) is the leading cause of severe visual impairment in the elderly. The appearance of amyloid-β in eye tissues makes it possible to see in a new light the problem of eye amyloidosis. Amyloidosis and aging is fundamental biological problem. The appearance of amyloid-β in eye tissues is related with development of some gerontoophtalmological diseases. Histological, immunohistochemical, and electron microscopic studies of the 137 eyes with AMD revealed amyloid-β in the drusen, Bruch’s membrane, and between the basal membrane of the retinal pigment epithelium (RPE) and internal collagen layer of Bruch’s membrane. Comparative analysis of morphological changes in tissues of the macular and paramacular areas and the incidence of amyloid-β incorporations in them permit us to propose that accumulation of local senile amyloid-β is conductive to development and aggravation of AMD. Ultrastructural studies of Bruch’s membrane in the macular region have shown that amyloid-β fibrills are localized in inner collagenous zones of Bruch’s membrane with fragments of degrading RPE cells closely attached to them. By reason not clear yet, a portion of the damaged photoreceptor membrane material resists the enzymatic digestion. The fact results in partial degradation, autophagy and accumulating in the cytoplasm of RPE cells of some material except lipids out of which amyliod-β fibrils may be formed. The authors put forward a hypothesis of the pathogenesis of AMD, in which the principal role in the formation and deposition of abnormal protein-amyloid-β, is played by degenerative cells of RPE.