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We hypothesized that this vulnerability would manifest as altered A\u03b2\u2013myelin coupling in preclinical Alzheimer's disease (AD).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>We assessed spatial coupling between amyloid positron emission tomography (PET) and myelin content estimated from T1w\/T2w ratio maps in 151 cognitively unimpaired older adults. Associations with preclinical AD, blood\u2010based biomarkers, resting\u2010state functional connectivity (rs\u2010FC), and subjective memory complaints (SMC) were examined.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      Compared with controls, A\u03b2\n                      <jats:sup>+<\/jats:sup>\n                      individuals exhibited increased positive and negative A\u03b2\u2013myelin coupling in late\u2010 and early\u2010myelinating regions, respectively, likely reflecting compensatory remyelination versus progressive myelin loss, along with disrupted rs\u2010FC and greater SMC. Serum glial fibrillary acidic protein (GFAP) and plasma phosphorylated tau at threonine 181 (pTau\u2010181) showed differential, region\u2010specific associations with A\u03b2\u2013myelin coupling, with GFAP partially mediating tau\u2010related effects. Exploratory stratification suggested distinct biomarker profiles linked to the direction of coupling dominance, potentially reflecting different preclinical AD phases.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>A\u03b2\u2013myelin coupling may represent a sensitive, stage\u2010dependent marker of early AD\u2013related cortical pathology.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.71268","type":"journal-article","created":{"date-parts":[[2026,3,9]],"date-time":"2026-03-09T04:28:18Z","timestamp":1773030498000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["In vivo mapping of cortical amyloid beta\u2010myelin coupling in preclinical Alzheimer's disease"],"prefix":"10.1002","volume":"22","author":[{"given":"Mercedes","family":"Atienza","sequence":"first","affiliation":[{"name":"Laboratory of Functional Neuroscience Pablo de Olavide University  Seville Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Enfermedades Neurodegenerativas (CIBERNED) Instituto de Salud Carlos III  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jose L.","family":"Cantero","sequence":"additional","affiliation":[{"name":"Laboratory of Functional Neuroscience Pablo de Olavide University  Seville Spain"},{"name":"Centro de Investigaci\u00f3n Biom\u00e9dica en Red de Enfermedades Neurodegenerativas (CIBERNED) Instituto de Salud Carlos III  Madrid 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