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

Published

Journal Article

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.

Full Text

Duke Authors

Cited Authors

  • Ridge, PG; Hoyt, KB; Boehme, K; Mukherjee, S; Crane, PK; Haines, JL; Mayeux, R; Farrer, LA; Pericak-Vance, MA; Schellenberg, GD; Kauwe, JSK; Alzheimer's Disease Genetics Consortium (ADGC),

Published Date

  • May 2016

Published In

Volume / Issue

  • 41 /

Start / End Page

  • 200.e13 - 200.e20

PubMed ID

  • 27036079

Pubmed Central ID

  • 27036079

Electronic International Standard Serial Number (EISSN)

  • 1558-1497

Digital Object Identifier (DOI)

  • 10.1016/j.neurobiolaging.2016.02.024

Language

  • eng

Conference Location

  • United States