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In Alzheimer's disease (AD), the link between tau aggregation and myelin integrity remains unclear, despite the preferential emergence of tau pathology in late\u2010myelinating regions. Here, we propose a myelin\u2010centered framework for tau pathology based on three mechanisms. First, vulnerability of late\u2010myelinating oligodendrocytes may drive myelin breakdown, metabolic stress, and axonal dysfunction, promoting tau hyperphosphorylation. Second, microglial responses to myelin injury may become maladaptive, with lipid overload impairing tau clearance. Third, oligodendrocytes may act as conditional reservoirs facilitating tau propagation across myelinated networks. Together, these processes suggest that myelin loss may contribute to tau accumulation, clearance deficits, and spread, providing a framework for future experimental testing. This perspective highlights myelin biology as a source of new conceptual insights and therapeutic strategies in AD.<\/jats:p>","DOI":"10.1002\/alz.71774","type":"journal-article","created":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T05:57:38Z","timestamp":1787205458000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["When myelin breaks, tau aggregates \u2014 a new perspective on Alzheimer's disease"],"prefix":"10.1002","volume":"22","author":[{"given":"Assia","family":"Tiane","sequence":"first","affiliation":[{"name":"Department of Psychiatry and Neuropsychology, Mental Health and Neuroscience Research Institute (MHeNs) Maastricht University  Maastricht The Netherlands"},{"name":"Department of Neuroscience, Biomedical Research Institute, Faculty of Medicine and Life Sciences Hasselt University  Hasselt Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"van den 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