{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T08:20:11Z","timestamp":1793866811893,"version":"4.6.1"},"reference-count":47,"publisher":"American Medical Association (AMA)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Netw Open"],"abstract":"<jats:sec id=\"ab-zoi230423-4\"><jats:title>Importance<\/jats:title><jats:p>An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course. However, robust evidence for most of these risk factors is lacking. Effective interventions should target risk factors in the causal pathway to dementia.<\/jats:p><\/jats:sec><jats:sec id=\"ab-zoi230423-5\"><jats:title>Objective<\/jats:title><jats:p>To comprehensively disentangle potentially causal aspects of modifiable risk factors for Alzheimer disease (AD) to inspire new drug targeting and improved prevention.<\/jats:p><\/jats:sec><jats:sec id=\"ab-zoi230423-6\"><jats:title>Design, Setting, and Participants<\/jats:title><jats:p>This genetic association study was conducted using 2-sample univariable and multivariable mendelian randomization. Independent genetic variants associated with modifiable risk factors were selected as instrumental variables from genomic consortia. Outcome data for AD were obtained from the European Alzheimer &amp;amp;amp; Dementia Biobank (EADB), generated on August 31, 2021. Main analyses were conducted using the EADB clinically diagnosed end point data. All analyses were performed between April 12 and October 27, 2022.<\/jats:p><\/jats:sec><jats:sec id=\"ab-zoi230423-7\"><jats:title>Exposures<\/jats:title><jats:p>Genetically determined modifiable risk factors.<\/jats:p><\/jats:sec><jats:sec id=\"ab-zoi230423-8\"><jats:title>Main Outcomes and Measures<\/jats:title><jats:p>Odds ratios (ORs) and 95% CIs for AD were calculated per 1-unit change of genetically determined risk factors.<\/jats:p><\/jats:sec><jats:sec id=\"ab-zoi230423-9\"><jats:title>Results<\/jats:title><jats:p>The EADB-diagnosed cohort included 39\u202f106 participants with clinically diagnosed AD and 401\u202f577 control participants without AD. The mean age ranged from 72 to 83 years for participants with AD and 51 to 80 years for control participants. Among participants with AD, 54% to 75% were female, and among control participants, 48% to 60% were female. Genetically determined high-density lipoprotein (HDL) cholesterol concentrations were associated with increased odds of AD (OR per 1-SD increase, 1.10 [95% CI, 1.05-1.16]). Genetically determined high systolic blood pressure was associated with increased risk of AD after adjusting for diastolic blood pressure (OR per 10\u2013mm Hg increase, 1.22 [95% CI, 1.02-1.46]). In a second analysis to minimize bias due to sample overlap, the entire UK Biobank was excluded from the EADB consortium; odds for AD were similar for HDL cholesterol (OR per 1-SD unit increase, 1.08 [95% CI, 1.02-1.15]) and systolic blood pressure after adjusting for diastolic blood pressure (OR per 10\u2013mm Hg increase, 1.23 [95% CI, 1.01-1.50]).<\/jats:p><\/jats:sec><jats:sec id=\"ab-zoi230423-10\"><jats:title>Conclusions and Relevance<\/jats:title><jats:p>This genetic association study found novel genetic associations between high HDL cholesterol concentrations and high systolic blood pressure with higher risk of AD. These findings may inspire new drug targeting and improved prevention implementation.<\/jats:p><\/jats:sec>","DOI":"10.1001\/jamanetworkopen.2023.13734","type":"journal-article","created":{"date-parts":[[2023,5,17]],"date-time":"2023-05-17T15:03:41Z","timestamp":1684335821000},"page":"e2313734","source":"Crossref","is-referenced-by-count":75,"title":["Genetic Associations Between Modifiable Risk Factors and Alzheimer Disease"],"prefix":"10.1001","volume":"6","author":[{"name":"European Alzheimer\u2019s & Dementia Biobank Mendelian Randomization (EADB-MR) Collaboration","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jiao","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, Copenhagen University Hospital\u2013Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jesper Qvist","family":"Thomassen","sequence":"additional","affiliation":[{"name":"Department of Clinical Biochemistry, Copenhagen University Hospital\u2013Rigshospitalet, Copenhagen, Denmark"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00e9line","family":"Bellenguez","sequence":"additional","affiliation":[{"name":"Univ. Lille, Inserm, CHU Lille, Institut Pasteur Lille, U1167\u2013RID-AGE\u2013Facteurs de risque et d\u00e9terminants mol\u00e9culaires des maladies li\u00e9es au vieillissement, Lille, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin","family":"Grenier-Boley","sequence":"additional","affiliation":[{"name":"Univ. Lille, Inserm, CHU Lille, Institut Pasteur Lille, U1167\u2013RID-AGE\u2013Facteurs de risque et d\u00e9terminants mol\u00e9culaires des maladies li\u00e9es au vieillissement, Lille, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Itziar","family":"de Rojas","sequence":"additional","affiliation":[{"name":"Research Center and Memory clinic Fundaci\u00f3 ACE, Institut Catal\u00e0 de Neuroci\u00e8ncies Aplicades, Universitat Internacional de Catalunya, Barcelona, Spain"},{"name":"Network Center for Biomedical Research in Neurodegenerative Diseases, National Institute of Health Carlos III, Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Atahualpa","family":"Castillo","sequence":"additional","affiliation":[{"name":"Division of Psychological Medicine and Clinical Neuroscience, School of Medicine, Cardiff University, Wales, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kayenat","family":"Parveen","sequence":"additional","affiliation":[{"name":"Division of Neurogenetics and Molecular Psychiatry, Department of Psychiatry and Psychotherapy, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany"},{"name":"Department of Neurodegenerative diseases and Geriatric Psychiatry, University Hospital Bonn, Medical Faculty, Bonn, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fahri","family":"K\u00fc\u00e7\u00fckali","sequence":"additional","affiliation":[{"name":"Complex Genetics of Alzheimer's Disease Group, VIB Center for Molecular Neurology, Antwerp, Belgium"},{"name":"Department of Biomedical Sciences, University of Antwerp, Antwerp, Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aude","family":"Nicolas","sequence":"additional","affiliation":[{"name":"Univ. Lille, Inserm, CHU Lille, Institut Pasteur Lille, U1167\u2013RID-AGE\u2013Facteurs de risque et d\u00e9terminants mol\u00e9culaires des maladies li\u00e9es au vieillissement, Lille, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oliver","family":"Peters","sequence":"additional","affiliation":[{"name":"German Center for Neurodegenerative Diseases, Berlin, Germany"},{"name":"Institute of Psychiatry and Psychotherapy, Charit\u00e9\u2013Universit\u00e4tsmedizin Berlin, corporate member of Freie Universit\u00e4t Berlin, Humboldt\u2013Universit\u00e4t zu Berlin, and Berlin Institute of Health, Institute of Psychiatry and Psychotherapy, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anja","family":"Schneider","sequence":"additional","affiliation":[{"name":"German Center for Neurodegenerative Diseases, Bonn, Germany"},{"name":"Department for Neurodegenerative Diseases and Geriatric Psychiatry, University Hospital Bonn, Bonn, 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