title: A novel Alzheimer disease locus located near the gene encoding tau protein.
abstract: APOE ɛ4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. We re-analyzed genome-wide association study (GWAS) data from the International Genomics of Alzheimer's Project (IGAP) Consortium in APOE ɛ4+ (10 352 cases and 9207 controls) and APOE ɛ4- (7184 cases and 26 968 controls) subgroups as well as in the total sample testing for interaction between a single-nucleotide polymorphism (SNP) and APOE ɛ4 status. Suggestive associations (P<1 × 10(-4)) in stage 1 were evaluated in an independent sample (stage 2) containing 4203 subjects (APOE ɛ4+: 1250 cases and 536 controls; APOE ɛ4-: 718 cases and 1699 controls). Among APOE ɛ4- subjects, novel genome-wide significant (GWS) association was observed with 17 SNPs (all between KANSL1 and LRRC37A on chromosome 17 near MAPT) in a meta-analysis of the stage 1 and stage 2 data sets (best SNP, rs2732703, P=5·8 × 10(-9)). Conditional analysis revealed that rs2732703 accounted for association signals in the entire 100-kilobase region that includes MAPT. Except for previously identified AD loci showing stronger association in APOE ɛ4+ subjects (CR1 and CLU) or APOE ɛ4- subjects (MS4A6A/MS4A4A/MS4A6E), no other SNPs were significantly associated with AD in a specific APOE genotype subgroup. In addition, the finding in the stage 1 sample that AD risk is significantly influenced by the interaction of APOE with rs1595014 in TMEM106B (P=1·6 × 10(-7)) is noteworthy, because TMEM106B variants have previously been associated with risk of frontotemporal dementia. Expression quantitative trait locus analysis revealed that rs113986870, one of the GWS SNPs near rs2732703, is significantly associated with four KANSL1 probes that target transcription of the first translated exon and an untranslated exon in hippocampus (P ⩽ 1.3 × 10(-8)), frontal cortex (P ⩽ 1.3 × 10(-9)) and temporal cortex (P⩽1.2 × 10(-11)). Rs113986870 is also strongly associated with a MAPT probe that targets transcription of alternatively spliced exon 3 in frontal cortex (P=9.2 × 10(-6)) and temporal cortex (P=2.6 × 10(-6)). Our APOE-stratified GWAS is the first to show GWS association for AD with SNPs in the chromosome 17q21.31 region. Replication of this finding in independent samples is needed to verify that SNPs in this region have significantly stronger effects on AD risk in persons lacking APOE ɛ4 compared with persons carrying this allele, and if this is found to hold, further examination of this region and studies aimed at deciphering the mechanism(s) are warranted.
authors.affiliation: Department of Medicine (Biomedical Genetics), Boston University School of Medicine, Boston, MA, USA.|Department of Ophthalmology, Boston University School of Medicine, Boston, MA, USA.|Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA.
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authors.affiliation: Institute of Psychological Medicine and Clinical Neurosciences, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, UK.
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authors.affiliation: Inserm U744, Lille, France.|Université Lille 2, Lille, France.|Institut Pasteur de Lille, Lille, France.
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authors.affiliation: Department of Medicine (Biomedical Genetics), Boston University School of Medicine, Boston, MA, USA.
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authors.affiliation: Inserm U744, Lille, France.|Université Lille 2, Lille, France.|Institut Pasteur de Lille, Lille, France.
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authors.affiliation: Department of Epidemiology, Erasmus University Medical Center, Erasmus, Rotterdam,The Netherlands.|Netherlands Consortium for Healthy Aging, Leiden, The Netherlands.|Department of Radiology, Erasmus University Medical Center, Erasmus, Rotterdam,The Netherlands.
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authors.affiliation: Department of Neurology, Erasmus University Medical Center, Erasmus, Rotterdam,The Netherlands.|Program in Translational NeuroPsychiatric Genomics, Institute for the Neurosciences, Department of Neurology and Psychiatry, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA.|Program in Medical and Population Genetics, Broad Institute, Cambridge, MA, USA.
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authors.affiliation: Inserm U897, Victor Segalen University, F-33076, Bordeaux, France.|Centre de Mémoire de Ressources et de Recherche de Bordeaux, CHU de Bordeaux, Bordeaux, France.
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authors.affiliation: Arizona Alzheimer's Consortium, Phoenix, AZ, USA.|Department of Psychiatry, University of Arizona, Phoenix, AZ, USA.|Banner Alzheimer's Institute, Phoenix, AZ, USA.|Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Arizona.
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authors.affiliation: Taub Institute on Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA.|Gertrude H. Sergievsky Center, Columbia University, New York, NY, USA.|Department of Neurology, Columbia University, New York, NY, USA.
authors.forename: R
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authors.affiliation: Foundation Jean Dausset-CEPH, Paris, France.|Centre National de Genotypage, Institut Genomique, Commissariat a l'energie Atomique, Evry, France.|McGill University and Génome Québec Innovation Centre, Montreal, QC, Canada.
authors.forename: M
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authors.affiliation: Institute of Psychological Medicine and Clinical Neurosciences, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, UK.
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authors.affiliation: The John P. Hussman Institute for Human Genomics, University of Miami, Miami, FL, USA.|Macdonald Foundation Department of Human Genetics, University of Miami, Miami, FL, USA.
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authors.affiliation: Inserm U744, Lille, France.|Université Lille 2, Lille, France.|Institut Pasteur de Lille, Lille, France.|University Hospital, CHRU Lille, Lille, France.
authors.forename: P
authors.identifier: http://orcid.org/0000-0001-9088-234X
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authors.affiliation: Institute of Psychological Medicine and Clinical Neurosciences, Medical Research Council (MRC) Centre for Neuropsychiatric Genetics and Genomics, Cardiff University, Cardiff, UK.
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authors.affiliation: Department of Epidemiology, Erasmus University Medical Center, Erasmus, Rotterdam,The Netherlands.
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authors.forename: G D
authors.initials: GD
authors.lastname: Schellenberg
authors.affiliation: Department of Medicine (Biomedical Genetics), Boston University School of Medicine, Boston, MA, USA.|Department of Ophthalmology, Boston University School of Medicine, Boston, MA, USA.|Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA.|Department of Neurology, Boston University School of Medicine, Boston, MA, USA.|Department of Epidemiology, Boston University School of Public Health, Boston, MA, USA.
authors.forename: L A
authors.initials: LA
authors.lastname: Farrer
mesh_terms: D000544:Alzheimer Disease / Q000235:genetics*; D053327:Apolipoprotein E4 / Q000235:genetics; D002886:Chromosomes, Human, Pair 17; D055106:Genome-Wide Association Study; D006801:Humans; D020641:Polymorphism, Single Nucleotide; D016875:tau Proteins / Q000235:genetics
chemical_list: D053327:Apolipoprotein E4; C054369:MAPT protein, human; D016875:tau Proteins