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Sorl1 as an Alzheimer’s Disease Predisposition Gene?Webster J.A.a · Myers A.J.b · Pearson J.V.a · Craig D.W.a · Hu-Lince D.a · Coon K.D.a · Zismann V.L.a · Beach T.c, d · Leung D.e · Bryden L.e · Halperin R.F.a · Marlowe L.e · Kaleem M.e · Huentelman M.J.a · Joshipura K.a · Walker D.c, d · Heward C.B.f · Ravid R.i · Rogers J.c, d · Papassotiropoulos A.a, j · Hardy J.b · Reiman E.M.a, d, g, h · Stephan D.A.a, d
aNeurogenomics Division, Translational Genomics Research Institute, Phoenix, Ariz.; bDepartment of Psychiatry and Behavioral Sciences, University of Miami, Miller School of Medicine, Miami, Fla.; cSun Health Research Institute, Sun City, Ariz.; dArizona Alzheimer’s Consortium, Phoenix, Ariz.; eLaboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Md.; fKronos Science Laboratories, gBanner Alzheimer’s Institute, Phoenix, Ariz., and hDepartment of Psychiatry, University of Arizona, Tucson, Ariz., USA; iRoyal Dutch Academy of Sciences, Amsterdam, The Netherlands; jDivision of Psychiatry Research, University of Zurich, Zurich, Switzerland
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressively disabling impairments in memory, cognition, and non-cognitive behavioural symptoms. Sporadic AD is multifactorial and genetically complex. While several monogenic mutations cause early-onset AD and gene alleles have been suggested as AD susceptibility factors, the only extensively validated susceptibility gene for late-onset AD is the apolipoprotein E (APOE) Ε4 allele. Alleles of the APOE gene do not account for all of the genetic load calculated to be responsible for AD predisposition. Recently, polymorphisms across the neuronal sortilin-related receptor (SORL1) gene were shown to be significantly associated with AD in several cohorts. Here we present the results of our large case-control whole-genome scan at over 500,000 polymorphisms which presents weak evidence for association and potentially narrows the association interval.
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