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. 2016 May:41:200.e13-200.e20.
doi: 10.1016/j.neurobiolaging.2016.02.024. Epub 2016 Mar 3.

Assessment of the genetic variance of late-onset Alzheimer's disease

Perry G Ridge  1 , Kaitlyn B Hoyt  1 , Kevin Boehme  1 , Shubhabrata Mukherjee  2 , Paul K Crane  2 , Jonathan L Haines  3 , Richard Mayeux  4 , Lindsay A Farrer  5 , Margaret A Pericak-Vance  6 , Gerard D Schellenberg  7 , John S K Kauwe  8 ; Alzheimer's Disease Genetics Consortium (ADGC)
Collaborators, Affiliations

Assessment of the genetic variance of late-onset Alzheimer's disease

Perry G Ridge et al. Neurobiol Aging. 2016 May.

Abstract

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.

Keywords: Alzheimer's disease; Genetic variance; Genetics.

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