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To address this and better characterize the genetic landscape of AD, we performed an in-depth X-Chromosome-Wide Association Study (XWAS) in 115,841 AD cases or AD proxy cases, including 52,214 clinically-diagnosed AD cases, and 613,671 controls. We considered three approaches to account for the different X-chromosome inactivation (XCI) states in females, i.e. random XCI, skewed XCI, and escape XCI. We did not detect any genome-wide significant signals (P\u2009\u2264\u20095\u2009\u00d7\u200910<jats:sup>\u2212<\/jats:sup>\n            <jats:sup>8<\/jats:sup>) but identified seven X-chromosome-wide significant loci (P\u2009\u2264\u20091.6\u2009\u00d7\u200910<jats:sup>\u2212<\/jats:sup>\n            <jats:sup>6<\/jats:sup>). The index variants were common for the Xp22.32, <jats:italic>FRMPD4, DMD<\/jats:italic> and Xq25 loci, and rare for the <jats:italic>WNK3<\/jats:italic>, <jats:italic>PJA1<\/jats:italic>, and <jats:italic>DACH2<\/jats:italic> loci. Overall, this well-powered XWAS found no genetic risk factors for AD on the non-pseudoautosomal region of the X-chromosome, but it identified suggestive signals warranting further investigations.<\/jats:p>","DOI":"10.1038\/s41380-024-02838-5","type":"journal-article","created":{"date-parts":[[2024,12,4]],"date-time":"2024-12-04T14:18:18Z","timestamp":1733321898000},"page":"2335-2346","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":14,"title":["X\u2010chromosome-wide association study for Alzheimer\u2019s disease"],"prefix":"10.1038","volume":"30","author":[{"given":"Julie","family":"Le 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Study protocols for all cohorts were reviewed and approved by the appropriate institutional review boards.","order":2,"name":"Ethics","group":{"name":"EthicsHeading","label":"Ethics approval and consent to participate"}}]}}