{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T13:06:57Z","timestamp":1792674417135,"version":"4.5.0"},"reference-count":113,"publisher":"American Society for Clinical Investigation","issue":"16","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2017,8,17]]},"abstract":"<jats:p>\n                    <jats:bold>BACKGROUND.<\/jats:bold>\n                    Noninvasive detection of Alzheimer\u2019s disease (AD) with high specificity and sensitivity can greatly facilitate identification of at-risk populations for earlier, more effective intervention. AD patients exhibit a myriad of retinal pathologies, including hallmark amyloid \u03b2-protein (A\u03b2) deposits.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>METHODS.<\/jats:bold>\n                    Burden, distribution, cellular layer, and structure of retinal A\u03b2 plaques were analyzed in flat mounts and cross sections of definite AD patients and controls (\n                    <jats:italic>n<\/jats:italic>\n                    = 37). In a proof-of-concept retinal imaging trial (\n                    <jats:italic>n<\/jats:italic>\n                    = 16), amyloid probe curcumin formulation was determined and protocol was established for retinal amyloid imaging in live patients.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>RESULTS.<\/jats:bold>\n                    Histological examination uncovered classical and neuritic-like A\u03b2 deposits with increased retinal A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    plaques (4.7-fold;\n                    <jats:italic>P<\/jats:italic>\n                    = 0.0063) and neuronal loss (\n                    <jats:italic>P<\/jats:italic>\n                    = 0.0023) in AD patients versus matched controls. Retinal A\u03b2 plaque mirrored brain pathology, especially in the primary visual cortex (\n                    <jats:italic>P<\/jats:italic>\n                    = 0.0097 to\n                    <jats:italic>P<\/jats:italic>\n                    = 0.0018; Pearson\u2019s\n                    <jats:italic>r<\/jats:italic>\n                    = 0.84\u20130.91). Retinal deposits often associated with blood vessels and occurred in hot spot peripheral regions of the superior quadrant and innermost retinal layers. Transmission electron microscopy revealed retinal A\u03b2 assembled into protofibrils and fibrils. Moreover, the ability to image retinal amyloid deposits with solid-lipid curcumin and a modified scanning laser ophthalmoscope was demonstrated in live patients. A fully automated calculation of the retinal amyloid index (RAI), a quantitative measure of increased curcumin fluorescence, was constructed. Analysis of RAI scores showed a 2.1-fold increase in AD patients versus controls (\n                    <jats:italic>P<\/jats:italic>\n                    = 0.0031).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>CONCLUSION.<\/jats:bold>\n                    The geometric distribution and increased burden of retinal amyloid pathology in AD, together with the feasibility to noninvasively detect discrete retinal amyloid deposits in living patients, may lead to a practical approach for large-scale AD diagnosis and monitoring.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>FUNDING.<\/jats:bold>\n                    National Institute on Aging award (AG044897) and The Saban and The Marciano Family Foundations.\n                  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