{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T16:31:20Z","timestamp":1787070680693,"version":"build-2736575974"},"reference-count":376,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","license":[{"start":{"date-parts":[[2025,8,13]],"date-time":"2025-08-13T00:00:00Z","timestamp":1755043200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0 http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:p>Alzheimer\u2019s disease is a devastating neurodegenerative disorder affecting millions worldwide, with current treatments offering only limited benefits. Central to emerging research is the role of autophagy and endolysosomal pathways, which are essential for clearing misfolded proteins and damaged organelles. Bridging integrator 1 (BIN1), traditionally recognized for its role in membrane remodeling and endocytosis, has recently emerged as a top genetic risk factor for Alzheimer\u2019s disease, linking cellular clearance mechanisms to the development of toxic amyloid-beta plaques and tau tangles. In this review, we provide an accessible overview of how disruptions in autophagy and endolysosomal trafficking contribute to the neurodegeneration process in Alzheimer\u2019s disease, positioning BIN1 as a central mediator within this complex network. Recent advances have shown that alterations in BIN1 expression and isoform distribution are associated with increased tau pathology and changes in amyloid-beta processing. Moreover, BIN1 appears to also influence synaptic transmission, neuroinflammation, and overall cellular homeostasis. The integration of recent findings not only deepens our understanding of Alzheimer\u2019s disease pathology but also opens new avenues for the development of targeted treatments. This timely perspective underscores the potential of modulating BIN1 activity to enhance cellular clearance mechanisms and offers hope for more effective interventions for Alzheimer\u2019s disease.<\/jats:p>","DOI":"10.4103\/nrr.nrr-d-25-00243","type":"journal-article","created":{"date-parts":[[2025,8,14]],"date-time":"2025-08-14T08:00:11Z","timestamp":1755158411000},"page":"2899-2911","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["Bridging autophagy and endolysosomal dysfunction: Role of bridging integrator 1 in Alzheimer\u2019s disease"],"prefix":"10.4103","volume":"21","author":[{"given":"Julia","family":"Duckhorn","sequence":"first","affiliation":[{"name":"Department of Molecular Biology, Cell Biology and Biochemistry, Center for Translational Neuroscience, Carney Institute for Brain Science and Brown Institute for Translational Science, Brown University, Providence, RI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Doo Kyung","family":"Kim","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Cell Biology and Biochemistry, Center for Translational Neuroscience, Carney Institute for Brain Science and Brown Institute for Translational Science, Brown University, Providence, RI, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-4082-8008","authenticated-orcid":false,"given":"Yu-Wen Alvin","family":"Huang","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology, Cell Biology and Biochemistry, Center for Translational Neuroscience, Carney Institute for Brain Science and Brown Institute for Translational Science, Brown University, Providence, RI, 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