| Literature DB >> 25189118 |
Minerva M Carrasquillo1, Julia E Crook2, Otto Pedraza3, Colleen S Thomas2, V Shane Pankratz4, Mariet Allen1, Thuy Nguyen1, Kimberly G Malphrus1, Li Ma1, Gina D Bisceglio1, Rosebud O Roberts5, John A Lucas3, Glenn E Smith6, Robert J Ivnik6, Mary M Machulda6, Neill R Graff-Radford7, Ronald C Petersen8, Steven G Younkin1, Nilüfer Ertekin-Taner9.
Abstract
We tested association of nine late-onset Alzheimer's disease (LOAD) risk variants from genome-wide association studies (GWAS) with memory and progression to mild cognitive impairment (MCI) or LOAD (MCI/LOAD) in older Caucasians, cognitively normal at baseline and longitudinally evaluated at Mayo Clinic Rochester and Jacksonville (n>2000). Each variant was tested both individually and collectively using a weighted risk score. APOE-e4 associated with worse baseline memory and increased decline with highly significant overall effect on memory. CLU-rs11136000-G associated with worse baseline memory and incident MCI/LOAD. MS4A6A-rs610932-C associated with increased incident MCI/LOAD and suggestively with lower baseline memory. ABCA7-rs3764650-C and EPHA1-rs11767557-A associated with increased rates of memory decline in subjects with a final diagnosis of MCI/LOAD. PICALM-rs3851179-G had an unexpected protective effect on incident MCI/LOAD. Only APOE-inclusive risk scores associated with worse memory and incident MCI/LOAD. The collective influence of the nine top LOAD GWAS variants on memory decline and progression to MCI/LOAD appears limited. Discovery of biologically functional variants at these loci may uncover stronger effects on memory and incident disease.Entities:
Keywords: Alzheimer's disease; Association; Cognitive decline; Genetic risk; Memory; Mild cognitive impairment
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Year: 2014 PMID: 25189118 PMCID: PMC4268433 DOI: 10.1016/j.neurobiolaging.2014.07.042
Source DB: PubMed Journal: Neurobiol Aging ISSN: 0197-4580 Impact factor: 4.673