{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T09:38:58Z","timestamp":1791279538989,"version":"4.1.0"},"reference-count":212,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2025,8,4]],"date-time":"2025-08-04T00:00:00Z","timestamp":1754265600000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["alz-journals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alzheimer's &amp;amp; Dementia"],"published-print":{"date-parts":[[2025,8]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:label\/><jats:p>Diabetic retinopathy (DR) and Alzheimer's disease (AD) are progressive neurodegenerative disorders affecting the eye and the brain, respectively. Despite targeting different organs, they share common molecular mechanisms. A central process connecting these conditions is the unfolded protein response (UPR), which maintains protein homeostasis in the endoplasmic reticulum (ER). Dysregulation of UPR pathways, particularly the IRE1\u2010XBP1 and PERK\u2010eIF2\u03b1 pathways, can lead to inflammation, oxidative stress, and neurodegeneration. While the IRE1\u2010XBP1 pathway regulates protein folding and inflammatory signaling, the PERK\u2010eIF2\u03b1 pathway reduces protein synthesis but may trigger apoptosis if persistently activated. Emerging therapies targeting UPR pathways and ER chaperones show promise in mitigating neurodegenerative damage in DR and AD. This review highlights shared pathophysiological mechanisms, explore retinal biomarkers for early AD detection, and emphasizes UPR modulation as a therapeutic strategy for neurodegeneration in aging\u2010related diseases.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>Diabetic retinopathy (DR, ocular disorder) and Alzheimer's disease (AD, cerebral disorder) share common molecular mechanisms, including oxidative stress, inflammation, and proteostasis dysfunction.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>UPR is a critical pathway linking both diseases through endoplasmic reticulum (ER) stress and neurodegeneration and targeting unfolded protein response (UPR) pathways, ER chaperones (e.g., P58IPK), and anti\u2010inflammatory treatments show promise.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The IRE1\u2010XBP1 pathway regulates protein homeostasis and inflammation; XBP1s protects against ER stress in both retinal and brain neurons.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The PERK\u2010eIF2\u03b1 pathway suppresses protein synthesis under stress but may induce apoptosis via ATF4 and CHOP if chronically activated.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Age\u2010related decline in metabolism, proteostasis, and neurovascular function intensifies disease progression and exacerbates molecular and cellular damage in both DR and AD.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.70497","type":"journal-article","created":{"date-parts":[[2025,8,5]],"date-time":"2025-08-05T03:33:11Z","timestamp":1754364791000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["Diabetic retinopathy and Alzheimer's disease: Convergence of the unfolded protein response in neurodegeneration"],"prefix":"10.1002","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1532-7527","authenticated-orcid":false,"given":"Adri\u00e1n G.","family":"Palacios","sequence":"first","affiliation":[{"name":"Instituto de Neurociencia and Centro Interdisciplinario de Neurociencia de Valpara\u00edso, Facultad de Ciencias Universidad de Valpara\u00edso  Valparaiso Chile"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7848-3263","authenticated-orcid":false,"given":"Sarah X.","family":"Zhang","sequence":"additional","affiliation":[{"name":"Departments of Ophthalmology and Biochemistry, Ross Eye Institute University at Buffalo, State University of New York  Buffalo New York USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5018-339X","authenticated-orcid":false,"given":"M\u00f3nica L.","family":"Acosta","sequence":"additional","affiliation":[{"name":"New Zealand National 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