{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T19:07:43Z","timestamp":1788548863096,"version":"build-2803163510"},"reference-count":189,"publisher":"MDPI AG","issue":"5","license":[{"start":{"date-parts":[[2021,2,26]],"date-time":"2021-02-26T00:00:00Z","timestamp":1614297600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Amyloid-\u03b2 (A\u03b2) accumulations have been identified in the retina for neurodegeneration-associated disorders like Alzheimer\u2019s disease (AD), glaucoma, and age-related macular degeneration (AMD). Elevated retinal A\u03b2 levels were associated with progressive retinal neurodegeneration, elevated cerebral A\u03b2 accumulation, and increased disease severity with a decline in cognition and vision. Retinal A\u03b2 accumulation and its pathological effects were demonstrated to occur prior to irreversible neurodegeneration, which highlights its potential in early disease detection and intervention. Using the retina as a model of the brain, recent studies have focused on characterizing retinal A\u03b2 to determine its applicability for population-based screening of AD, which warrants a further understanding of how A\u03b2 manifests between these disorders. While current treatments directly targeting A\u03b2 accumulations have had limited results, continued exploration of A\u03b2-associated pathological pathways may yield new therapeutic targets for preserving cognition and vision. Here, we provide a review on the role of retinal A\u03b2 manifestations in these distinct neurodegeneration-associated disorders. We also discuss the recent applications of retinal A\u03b2 for AD screening and current clinical trial outcomes for A\u03b2-associated treatment approaches. Lastly, we explore potential future therapeutic targets based on overlapping mechanisms of pathophysiology in AD, glaucoma, and AMD.<\/jats:p>","DOI":"10.3390\/ijms22052360","type":"journal-article","created":{"date-parts":[[2021,2,26]],"date-time":"2021-02-26T21:02:34Z","timestamp":1614373354000},"page":"2360","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":81,"title":["Role of Retinal Amyloid-\u03b2 in Neurodegenerative Diseases: Overlapping Mechanisms and Emerging Clinical Applications"],"prefix":"10.3390","volume":"22","author":[{"given":"Liang","family":"Wang","sequence":"first","affiliation":[{"name":"Miller School of Medicine, University of Miami, Miami, FL 33136, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6587-556X","authenticated-orcid":false,"given":"Xiaobo","family":"Mao","sequence":"additional","affiliation":[{"name":"Neuroregeneration and Stem Cell Programs, Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA"},{"name":"Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2021,2,26]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","first-page":"52","DOI":"10.1016\/j.neulet.2016.04.059","article-title":"Amyloid beta accumulation and inner retinal degenerative changes in Alzheimer\u2019s disease transgenic mouse","volume":"623","author":"Gupta","year":"2016","journal-title":"Neurosci. 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