{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"medRxiv"}],"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T01:38:29Z","timestamp":1791941909710,"version":"4.3.4"},"posted":{"date-parts":[[2025,5,9]]},"group-title":"Genetic and Genomic Medicine","reference-count":48,"publisher":"openRxiv","license":[{"start":{"date-parts":[[2025,5,9]],"date-time":"2025-05-09T00:00:00Z","timestamp":1746748800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2025,12,19]]},"abstract":"<jats:p>\n                  Among the more than 90 identified genetic risk loci for late-onset Alzheimer\u2019s disease (AD) and related dementias, the apolipoprotein E gene (\n                  <jats:italic>APOE<\/jats:italic>\n                  ) \u025b2\/\u025b3\/\u025b4 polymorphisms remains the longstanding benchmark for genetic disease risk with a consistently large effect across studies\n                  <jats:sup>1\u201310<\/jats:sup>\n                  . Despite this massive signal, the exact mechanisms for how \u025b4 increases and for how \u025b2 decreases dementia risk is not well-understood. Importantly, recent trials of anti-amyloid therapies suggest less efficacy and higher risks of severe side effects in \u03b54 carriers\n                  <jats:sup>11\u201313<\/jats:sup>\n                  , hampering the treatment of those with the highest unmet need. To improve our understanding of the genetic architecture of AD in the context of its main genetic driver, we performed genome-wide association studies (GWASs) stratified by \u03b54 and \u03b52 carrier status. Such insights may help to understand and overcome side effects, to impact clinical trial enrolment strategies, and to create the scientific basis for targeted mechanism-driven therapies in neurodegenerative diseases.\n                <\/jats:p>","DOI":"10.1101\/2025.05.07.25327065","type":"posted-content","created":{"date-parts":[[2025,5,9]],"date-time":"2025-05-09T18:25:15Z","timestamp":1746815115000},"source":"Crossref","is-referenced-by-count":5,"title":["<i>APOE<\/i>\n                  stratified genome-wide association studies provide novel insights into the genetic etiology of Alzheimers\u2019s disease"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3484-9531","authenticated-orcid":false,"given":"Jesper Qvist","family":"Thomassen","sequence":"first","affiliation":[{"name":"Department of Clinical Biochemistry, Copenhagen University Hospital - Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, 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