{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T09:13:08Z","timestamp":1791191588299,"version":"4.1.0"},"reference-count":67,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2014,5,1]],"date-time":"2014-05-01T00:00:00Z","timestamp":1398902400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American J of Med Genetics Pt B"],"published-print":{"date-parts":[[2014,6]]},"abstract":"<jats:sec><jats:label\/><jats:p>Deviations from normal body weight are observed prior to and after the onset of Alzheimer's disease (AD). Midlife obesity confers increased AD risk in later life, whereas late\u2010life obesity is associated with decreased AD risk. The role of underweight and weight loss for AD risk is controversial. Based on the hypothesis of shared genetic variants for both obesity and AD, we analyzed the variants identified for AD or obesity from genome\u2010wide association meta\u2010analyses of the GERAD (AD, cases\u2009=\u20096,688, controls\u2009=\u200913,685) and GIANT (body mass index [BMI] as measure of obesity, n\u2009=\u2009123,865) consortia. Our cross\u2010disorder analysis of genome\u2010wide significant 39 obesity SNPs and 23 AD SNPs in these two large data sets revealed that: (1) The AD SNP rs10838725 (p<jats:sub>AD<\/jats:sub>\u2009=\u20091.1\u2009\u00d7\u200910<jats:sup>\u221208<\/jats:sup>) at the locus <jats:italic>CELF1<\/jats:italic> is also genome\u2010wide significant for obesity (p<jats:sub>BMI<\/jats:sub>\u2009=\u20097.35\u2009\u00d7\u200910<jats:sup>\u221209<\/jats:sup>). (2) Four additional AD risk SNPs were nominally associated with obesity (rs17125944 at <jats:italic>FERMT2<\/jats:italic>, p<jats:sub>BMI<\/jats:sub>\u2009=\u20094.03\u2009\u00d7\u200910<jats:sup>\u221205<\/jats:sup>, p<jats:sub>BMI\u2009corr<\/jats:sub>\u2009=\u20092.50\u2009\u00d7\u200910<jats:sup>\u221203<\/jats:sup>; rs3851179 at <jats:italic>PICALM<\/jats:italic>; p<jats:sub>BMI<\/jats:sub>\u2009=\u20090.002, rs2075650 at <jats:italic>TOMM40<\/jats:italic>\/<jats:italic>APOE<\/jats:italic>, p<jats:sub>BMI<\/jats:sub>\u2009=\u20090.024, rs3865444 at <jats:italic>CD33<\/jats:italic>, p<jats:sub>BMI<\/jats:sub>\u2009=\u20090.024). (3) SNPs at two of the obesity risk loci (rs4836133 downstream of <jats:italic>ZNF608<\/jats:italic>; p<jats:sub>AD<\/jats:sub>\u2009=\u20090.002 and at rs713586 downstream of <jats:italic>RBJ<\/jats:italic>\/<jats:italic>DNAJC27<\/jats:italic>; p<jats:sub>AD<\/jats:sub>\u2009=\u20090.018) were nominally associated with AD risk. Additionally, among the SNPs used for confirmation in both studies the AD risk allele of rs1858973, with an AD association just below genome\u2010wide significance (p<jats:sub>AD<\/jats:sub>\u2009=\u20097.20\u2009\u00d7\u200910<jats:sup>\u221207<\/jats:sup>), was also associated with obesity (SNP at <jats:italic>IQCK<\/jats:italic>\/<jats:italic>GPRC5B<\/jats:italic>; p<jats:sub>BMI<\/jats:sub>\u2009=\u20095.21\u2009\u00d7\u200910<jats:sup>\u221206<\/jats:sup>; p<jats:sub>corr<\/jats:sub>\u2009=\u20093.24\u2009\u00d7\u200910<jats:sup>\u221204<\/jats:sup>). Our first GWAS based cross\u2010disorder analysis for AD and obesity suggests that rs10838725 at the locus <jats:italic>CELF1<\/jats:italic> might be relevant for both disorders. \u00a9 2014 Wiley Periodicals, Inc.<\/jats:p><\/jats:sec>","DOI":"10.1002\/ajmg.b.32234","type":"journal-article","created":{"date-parts":[[2014,5,1]],"date-time":"2014-05-01T07:03:53Z","timestamp":1398927833000},"page":"283-293","source":"Crossref","is-referenced-by-count":43,"title":["Genetic variation at the <i>CELF1<\/i> (CUGBP, elav\u2010like family member 1 gene) locus is genome\u2010wide associated with Alzheimer's disease and obesity"],"prefix":"10.1002","volume":"165","author":[{"given":"Anke","family":"Hinney","sequence":"first","affiliation":[{"name":"Department of Child and Adolescent Psychiatry, Psychotherapy, and Psychosomatics Universit\u00e4tsklinikum Essen University of Duisburg\u2010Essen Essen 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Care (CSCC) Jena University Hospital Jena Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jens","family":"Wiltfang","sequence":"additional","affiliation":[{"name":"Department of Psychiatry and Psychotherapy Universit\u00e4tsklinikum Essen University of Duisburg\u2010Essen Essen Germany"},{"name":"Psychiatrische Klinik Universit\u00e4tsklinikum G\u00f6ttingen G\u00f6ttingen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julie","family":"Williams","sequence":"additional","affiliation":[{"name":"Institute of Psychological Medicine and Clinical Neurosciences MRC Centre for Neuropsychiatric Genetics and Genomics Cardiff University Henry Wellcome Building Heath Park Cardiff UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johannes","family":"Hebebrand","sequence":"additional","affiliation":[{"name":"Department of Child and Adolescent Psychiatry, Psychotherapy, and Psychosomatics Universit\u00e4tsklinikum Essen University 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