{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"institution":[{"name":"medRxiv"}],"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T12:17:29Z","timestamp":1768565849313,"version":"3.49.0"},"posted":{"date-parts":[[2023,11,7]]},"group-title":"Genetic and Genomic Medicine","reference-count":52,"publisher":"openRxiv","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"accepted":{"date-parts":[[2023,11,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                <jats:p>Alzheimer\u2019s disease (AD) is the most prevalent neurodegenerative disease worldwide, with one in nine people over the age of 65 living with the disease in 2023. In this study, we used a phenome wide association study (PheWAS) approach to identify cross-phenotype associations between previously identified genetic AD and for electronic health record (EHR) diagnoses from the UK Biobank (UKBB) (n=361,194 of European ancestry) and the eMERGE Network (n=105,108 of diverse ancestry). Based on 497 previously identified AD-associated variants from the Alzheimer\u2019s Disease Variant Portal (ADVP), we found significant associations primarily in immune and cardiac related diseases in our PheWAS. Replicating variants have widespread impacts on immune genes in diverse tissue types. This study demonstrates the potential of using the PheWAS strategy to improve our understanding of AD progression as well as identify potential drug repurposing opportunities for new treatment and disease prevention strategies.<\/jats:p>","DOI":"10.1101\/2023.11.06.23297993","type":"posted-content","created":{"date-parts":[[2023,11,7]],"date-time":"2023-11-07T15:25:59Z","timestamp":1699370759000},"source":"Crossref","is-referenced-by-count":0,"title":["Cross-phenotype associations between Alzheimer\u2019s Disease and its comorbidities may provide clues to progression"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1953-6449","authenticated-orcid":false,"given":"Anni","family":"Moore","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marylyn D.","family":"Ritchie","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"54368","reference":[{"key":"2023111003300522000_2023.11.06.23297993v1.1","doi-asserted-by":"publisher","DOI":"10.1002\/alz.13016"},{"key":"2023111003300522000_2023.11.06.23297993v1.2","doi-asserted-by":"publisher","DOI":"10.1016\/S0006-291X(84)80190-4"},{"key":"2023111003300522000_2023.11.06.23297993v1.3","doi-asserted-by":"publisher","DOI":"10.1016\/j.cell.2010.06.036"},{"issue":"6","key":"2023111003300522000_2023.11.06.23297993v1.4","first-page":"427","article-title":"Interactions between beta-amyloid and central cholinergic neurons: implications for Alzheimer\u2019s disease","volume":"29","year":"2004","journal-title":"J Psychiatry Neurosci"},{"key":"2023111003300522000_2023.11.06.23297993v1.5","doi-asserted-by":"publisher","DOI":"10.1001\/archpsyc.63.2.168"},{"issue":"3","key":"2023111003300522000_2023.11.06.23297993v1.6","doi-asserted-by":"crossref","first-page":"355","DOI":"10.1176\/appi.focus.19305","article-title":"When Does Alzheimer\u2019s Disease Really Start? 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