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There are no large genetic studies on early\u2010onset AD (EOAD).<\/jats:p><\/jats:sec><jats:sec><jats:title>METHODS<\/jats:title><jats:p>We performed a multi\u2010ancestry (non\u2010Hispanic European, African, and East Asian) genome\u2010wide association study (GWAS) including a total of 7,349 cases and 17,887 control. Cases with age at onset younger than 70 years were included. Sensitivity analysis including cases with onset\u00a0&lt;65 was performed. Only controls older than 70 were included to decrease the risk of developing LOAD.<\/jats:p><\/jats:sec><jats:sec><jats:title>RESULTS<\/jats:title><jats:p>We identified eight novel significant loci: six in the ancestry\u2010specific analyses and two in the trans\u2010ancestry analysis. By integrating gene\u2010based analysis, expression quantitative trait loci (eQTL), protein quantitative trait loci (pQTL), and functional annotations, we nominate eight novel genes that are involved in microglia activation, glutamate production, and signaling pathways.<\/jats:p><\/jats:sec><jats:sec><jats:title>DISCUSSION<\/jats:title><jats:p>EOAD, although sharing genes with LOAD, harbors unique genes and pathways that could be used to create better prediction models or target identification.<\/jats:p><\/jats:sec><jats:sec><jats:title>Highlights<\/jats:title><jats:p><jats:list list-type=\"bullet\">\n<jats:list-item><jats:p>We performed the largest and first multi\u2010ethnic genetic screening for early\u2010onset Alzheimer's disease (AD).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>We identified eight novel significant loci: six in the ancestry\u2010specific analyses and two in the trans\u2010ancestry analysis.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>The novel genes are implicated microglia activation, glutamate production, and signaling pathways.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>EOAD, although sharing many genes with LOAD, harbors unique genes and pathways that could be used to create better prediction models or target identification for this type of AD.<\/jats:p><\/jats:list-item>\n<\/jats:list><\/jats:p><\/jats:sec>","DOI":"10.1002\/alz.70377","type":"journal-article","created":{"date-parts":[[2025,6,25]],"date-time":"2025-06-25T01:24:14Z","timestamp":1750814654000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Novel early\u2010onset Alzheimer\u2010associated genes influence risk through dysregulation of glutamate, immune activation, and intracellular signaling pathways"],"prefix":"10.1002","volume":"21","author":[{"given":"Joseph","family":"Bradley","sequence":"first","affiliation":[{"name":"NeuroGenomics and Informatics Washington University School of Medicine  St. Louis Missouri USA"},{"name":"Department of Psychiatry Washington University in St. Louis  St Louis Missouri USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cyril","family":"Pottier","sequence":"additional","affiliation":[{"name":"NeuroGenomics and Informatics Washington University School of Medicine  St. Louis Missouri USA"},{"name":"Department of Psychiatry Washington University in St. Louis  St Louis Missouri USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eder Lucio","family":"da Fonseca","sequence":"additional","affiliation":[{"name":"The John P. 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