TY - JOUR
T1 - Assessment of the genetic variance of late-onset Alzheimer's disease
AU - Alzheimer's Disease Genetics Consortium (ADGC)
AU - Ridge, Perry G.
AU - Hoyt, Kaitlyn B.
AU - Boehme, Kevin
AU - Mukherjee, Shubhabrata
AU - Crane, Paul K.
AU - Haines, Jonathan L.
AU - Mayeux, Richard
AU - Farrer, Lindsay A.
AU - Pericak-Vance, Margaret A.
AU - Schellenberg, Gerard D.
AU - Kauwe, John S.K.
N1 - Publisher Copyright:
Copyright © 2016 The Authors. Published by Elsevier Inc. All rights reserved.
Copyright:
This record is sourced from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
PY - 2016/5/1
Y1 - 2016/5/1
N2 - Alzheimer's disease (AD) is a complex genetic disorder with no effective treatments. More than 20 common markers have been identified, which are associated with AD. Recently, several rare variants have been identified in Amyloid Precursor Protein (APP), Triggering Receptor Expressed On Myeloid Cells 2 (TREM2) and Unc-5 Netrin Receptor C (UNC5C) that affect risk for AD. Despite the many successes, the genetic architecture of AD remains unsolved. We used Genome-wide Complex Trait Analysis to (1) estimate phenotypic variance explained by genetics; (2) calculate genetic variance explained by known AD single nucleotide polymorphisms (SNPs); and (3) identify the genomic locations of variation that explain the remaining unexplained genetic variance. In total, 53.24% of phenotypic variance is explained by genetics, but known AD SNPs only explain 30.62% of the genetic variance. Of the unexplained genetic variance, approximately 41% is explained by unknown SNPs in regions adjacent to known AD SNPs, and the remaining unexplained genetic variance outside these regions.
AB - Alzheimer's disease (AD) is a complex genetic disorder with no effective treatments. More than 20 common markers have been identified, which are associated with AD. Recently, several rare variants have been identified in Amyloid Precursor Protein (APP), Triggering Receptor Expressed On Myeloid Cells 2 (TREM2) and Unc-5 Netrin Receptor C (UNC5C) that affect risk for AD. Despite the many successes, the genetic architecture of AD remains unsolved. We used Genome-wide Complex Trait Analysis to (1) estimate phenotypic variance explained by genetics; (2) calculate genetic variance explained by known AD single nucleotide polymorphisms (SNPs); and (3) identify the genomic locations of variation that explain the remaining unexplained genetic variance. In total, 53.24% of phenotypic variance is explained by genetics, but known AD SNPs only explain 30.62% of the genetic variance. Of the unexplained genetic variance, approximately 41% is explained by unknown SNPs in regions adjacent to known AD SNPs, and the remaining unexplained genetic variance outside these regions.
KW - Alzheimer's disease
KW - Genetic variance
KW - Genetics
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U2 - 10.1016/j.neurobiolaging.2016.02.024
DO - 10.1016/j.neurobiolaging.2016.02.024
M3 - Article
C2 - 27036079
AN - SCOPUS:85046579045
VL - 41
SP - 200.e13-20
JO - Neurobiology of Aging
JF - Neurobiology of Aging
SN - 0197-4580
ER -