{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T16:47:41Z","timestamp":1785257261227,"version":"3.55.0"},"reference-count":101,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2020,6,23]],"date-time":"2020-06-23T00:00:00Z","timestamp":1592870400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Journal of Alzheimer\u2019s Disease"],"published-print":{"date-parts":[[2020,8,4]]},"abstract":"<jats:sec>\n                    <jats:title>Background:<\/jats:title>\n                    <jats:p>Amyloid-\u03b2 soluble oligomers (A\u03b2o) are believed to be the cause of the pathophysiology underlying Alzheimer\u2019s disease (AD) and are normally detected some two decades before clinical onset of the disease. Retinal pathology associated with AD pathogenesis has previously been reported, including ganglion cell loss, accumulation of A\u03b2 deposits in the retina, and reduction of nerve fiber layer thickness as well as abnormalities of the microvasculature.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>This study\u2019s aim is to better understand the relationship between brain and retinal A\u03b2o deposition and in particular to quantify levels of the toxic A\u03b2o as a function of age in the retina of a rodent model of AD.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>Retinas and brain tissue from 5\u00d7FAD mice were stained with Congo red, Thioflavin-T (Th-T), and A\u03b2 plaque-specific and A\u03b2o-specific antibodies.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>We show that retinas displayed an age-dependent increase of Th-T-specific amyloid fibrils. Staining with anti-A\u03b2 antibody confirmed the presence of the A\u03b2 plaques in all 5\u00d7FAD retinas tested. In contrast, staining with anti-A\u03b2o antibody showed an age-dependent decrease of retinal A\u03b2o. Of note, A\u03b2o was observed mainly in the retinal nuclear layers. Finally, we confirmed the localization of A\u03b2o to neurons, typically accumulating in late endosomes, indicating possible impairment of the endocytic pathway.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>Our results demonstrate the presence of intraneuronal A\u03b2o in the retina and its accumulation inversely correlated with retinal A\u03b2 plaque deposition, indicating an age-related conversion in this animal model. These results support the development of an early AD diagnostic test targeting A\u03b2o in the eye.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3233\/jad-191346","type":"journal-article","created":{"date-parts":[[2020,6,23]],"date-time":"2020-06-23T11:01:56Z","timestamp":1592910116000},"page":"1135-1150","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":32,"title":["Age-Specific Retinal and Cerebral Immunodetection of Amyloid-\u03b2 Plaques and Oligomers in a Rodent Model of Alzheimer\u2019s Disease"],"prefix":"10.1177","volume":"76","author":[{"given":"Umma","family":"Habiba","sequence":"first","affiliation":[{"name":"School of Medicine, Western Sydney University, Campbelltown, NSW, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sam","family":"Merlin","sequence":"additional","affiliation":[{"name":"School of Science & Health, Western Sydney University, Campbelltown, NSW, 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