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Yet the mechanisms linking cognitive decline and skeletal deterioration remain poorly defined. Proteomic analysis of cortical bone from aged 21\u2010month\u2010old mice revealed strong enrichment of neurodegeneration\u2010associated proteins, including apolipoprotein E (Apoe) and amyloid precursor protein. Apoe localized specifically to osteocytes, with expression in aged female bone nearly twice that of young 4\u2010month\u2010old male bone. Because human APOE alleles confer different age\u2010related AD risks, we examined their roles in bone using humanized APOE2, APOE3, and APOE4 knock\u2010in mice and analyzed bone and hippocampus from the same animals. APOE4 produced marked sex\u2010specific effects on the bone transcriptome and proteome compared with APOE2 or APOE3. Strikingly, APOE4\u2010associated proteomic disruptions were stronger in female bone than in the hippocampus. Functionally, APOE4 caused bone fragility in females without altering cortical structure. These deficits stemmed from impaired osteocyte perilacunocanalicular remodeling. Our findings identify APOE4 as a molecular driver of early osteocyte dysfunction and reduced bone quality, disproportionately affecting females. These findings highlight osteocytes as potential targets for early diagnosis of age\u2010related cognitive impairment and treatment for bone fragility, in females.<\/jats:p>","DOI":"10.1002\/advs.202523511","type":"journal-article","created":{"date-parts":[[2026,4,13]],"date-time":"2026-04-13T11:50:17Z","timestamp":1776081017000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":3,"title":["Alzheimer's Disease Risk Factor APOE4 Exerts Dimorphic Effects on Female Bone"],"prefix":"10.1002","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-5739-8481","authenticated-orcid":false,"given":"Charles A.","family":"Schurman","sequence":"first","affiliation":[{"name":"Buck Institute for Research on Aging  Novato California 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