{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,3]],"date-time":"2026-11-03T17:29:56Z","timestamp":1793726996736,"version":"4.6.1"},"reference-count":66,"publisher":"American Medical Association (AMA)","issue":"10","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Neurol"],"published-print":{"date-parts":[[2024,10,1]]},"abstract":"<jats:sec id=\"ab-noi240054-4\"><jats:title>Importance<\/jats:title><jats:p>The X chromosome has remained enigmatic in Alzheimer disease (AD), yet it makes up 5% of the genome and carries a high proportion of genes expressed in the brain, making it particularly appealing as a potential source of unexplored genetic variation in AD.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi240054-5\"><jats:title>Objectives<\/jats:title><jats:p>To perform the first large-scale X chromosome\u2013wide association study (XWAS) of AD.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi240054-6\"><jats:title>Design, Setting, and Participants<\/jats:title><jats:p>This was a meta-analysis of genetic association studies in case-control, family-based, population-based, and longitudinal AD-related cohorts from the US Alzheimer\u2019s Disease Genetics Consortium, the Alzheimer\u2019s Disease Sequencing Project, the UK Biobank, the Finnish health registry, and the US Million Veterans Program. Risk of AD was evaluated through case-control logistic regression analyses. Data were analyzed between January 2023 and March 2024. Genetic data available from high-density single-nucleotide variant microarrays and whole-genome sequencing and summary statistics for multitissue expression and protein quantitative trait loci available from published studies were included, enabling follow-up genetic colocalization analyses. A total of 1\u202f629\u202f863 eligible participants were selected from referred and volunteer samples, 477\u202f596 of whom were excluded for analysis exclusion criteria. The number of participants who declined to participate in original studies was not available.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi240054-7\"><jats:title>Main Outcome and Measures<\/jats:title><jats:p>Risk of AD, reported as odds ratios (ORs) with 95% CIs. Associations were considered at X chromosome\u2013wide (<jats:italic>P<\/jats:italic>\u2009&amp;amp;lt;\u20091\u2009\u00d7\u200910<jats:sup>\u22125<\/jats:sup>) and genome-wide (<jats:italic>P<\/jats:italic>\u2009&amp;amp;lt;\u20095\u2009\u00d7\u200910<jats:sup>\u22128<\/jats:sup>) significance. Primary analyses are nonstratified, while secondary analyses evaluate sex-stratified effects.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi240054-8\"><jats:title>Results<\/jats:title><jats:p>Analyses included 1\u202f152\u202f284 participants of non-Hispanic White, European ancestry (664\u202f403 [57.7%] female and 487\u202f881 [42.3%] male), including 138\u202f558 individuals with AD. Six independent genetic loci passed X chromosome\u2013wide significance, with 4 showing support for links between the genetic signal for AD and expression of nearby genes in brain and nonbrain tissues. One of these 4 loci passed conservative genome-wide significance, with its lead variant centered on an intron of <jats:italic>SLC9A7<\/jats:italic> (OR, 1.03; 95% CI, 1.02-1.04) and colocalization analyses prioritizing both the <jats:italic>SLC9A7<\/jats:italic> and nearby <jats:italic>CHST7<\/jats:italic> genes. Of these 6 loci, 4 displayed evidence for escape from X chromosome inactivation with regard to AD risk.<\/jats:p><\/jats:sec><jats:sec id=\"ab-noi240054-9\"><jats:title>Conclusion and Relevance<\/jats:title><jats:p>This large-scale XWAS of AD identified the novel <jats:italic>SLC9A7<\/jats:italic> locus. <jats:italic>SLC9A7<\/jats:italic> regulates pH homeostasis in Golgi secretory compartments and is anticipated to have downstream effects on amyloid \u03b2 accumulation. Overall, this study advances our knowledge of AD genetics and may provide novel biological drug targets. The results further provide initial insights into elucidating the role of the X chromosome in sex-based differences in AD.<\/jats:p><\/jats:sec>","DOI":"10.1001\/jamaneurol.2024.2843","type":"journal-article","created":{"date-parts":[[2024,9,9]],"date-time":"2024-09-09T15:05:04Z","timestamp":1725894304000},"page":"1032","source":"Crossref","is-referenced-by-count":39,"title":["Role of the X Chromosome in Alzheimer Disease Genetics"],"prefix":"10.1001","volume":"81","author":[{"given":"Michael E.","family":"Belloy","sequence":"first","affiliation":[{"name":"Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California"},{"name":"NeuroGenomics and Informatics Center, Washington University School of Medicine, St Louis, Missouri"},{"name":"Department of Neurology, Washington University School of Medicine, St Louis, Missouri"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yann","family":"Le Guen","sequence":"additional","affiliation":[{"name":"Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California"},{"name":"Quantitative Sciences Unit, Department of Medicine, Stanford University School of Medicine, Stanford, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ilaria","family":"Stewart","sequence":"additional","affiliation":[{"name":"Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kennedy","family":"Williams","sequence":"additional","affiliation":[{"name":"Department of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joachim","family":"Herz","sequence":"additional","affiliation":[{"name":"Center for Translational Neurodegeneration Research, Department of Molecular Genetics University of Texas Southwestern Medical Center at Dallas, Dallas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard","family":"Sherva","sequence":"additional","affiliation":[{"name":"Biomedical Genetics, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Zhang","sequence":"additional","affiliation":[{"name":"National Center for PTSD, Behavioral Sciences Division, VA Boston Healthcare System, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Victoria","family":"Merritt","sequence":"additional","affiliation":[{"name":"Center of Excellence for Stress and Mental Health, VA San Diego Healthcare System, San Diego, California"},{"name":"Department of Psychiatry, University of California San Diego, La Jolla"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew S.","family":"Panizzon","sequence":"additional","affiliation":[{"name":"Department of Psychiatry, University of California San Diego, La Jolla"},{"name":"Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richard L.","family":"Hauger","sequence":"additional","affiliation":[{"name":"Center of Excellence for Stress and Mental Health, VA San Diego Healthcare System, San Diego, California"},{"name":"Department of Psychiatry, University of California San Diego, La Jolla"},{"name":"Center for Behavior Genetics of Aging, University of California, San Diego, La Jolla"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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