DESCRIPTION:

List of positional candidate genes after correcting for multiple testing and controlling the false discovery rate from genome wide association studies (GWAS) retrieved from the NHGRI-EBI Catalog of published genome-wide association studies (http://www.ebi.ac.uk/gwas/). The disease/trait examined in this study, as reported by the authors, was Cognitive function. The EFO term cognition was annotated to this set after curation by NHGRI-EBI. Intergenic SNPS were mapped to both the upstream and downstream gene. P-value uploaded. This gene set was generated using gwas2gs v. 0.1.8 and the GWAS Catalog v. 1.0.1.

LABEL:

GWAS: cognition

SCORE TYPE:

P-Value

DATE ADDED:

2017-05-02

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

G Davies, N Armstrong, JC Bis, J Bressler, V Chouraki, S Giddaluru, E Hofer, CA Ibrahim-Verbaas, M Kirin, J Lahti, SJ van der Lee, S Le Hellard, T Liu, RE Marioni, C Oldmeadow, I Postmus, AV Smith, JA Smith, A Thalamuthu, R Thomson, V Vitart, J Wang, L Yu, L Zgaga, W Zhao, R Boxall, SE Harris, WD Hill, DC Liewald, M Luciano, H Adams, D Ames, N Amin, P Amouyel, AA Assareh, R Au, JT Becker, A Beiser, C Berr, L Bertram, E Boerwinkle, BM Buckley, H Campbell, J Corley, PL De Jager, C Dufouil, JG Eriksson, T Espeseth, JD Faul, I Ford, RF Gottesman, ME Griswold, V Gudnason, TB Harris, G Heiss, A Hofman, EG Holliday, J Huffman, SL Kardia, N Kochan, DS Knopman, JB Kwok, JC Lambert, T Lee, G Li, SC Li, M Loitfelder, OL Lopez, AJ Lundervold, A Lundqvist, KA Mather, SS Mirza, L Nyberg, BA Oostra, A Palotie, G Papenberg, A Pattie, K Petrovic, O Polasek, BM Psaty, P Redmond, S Reppermund, JI Rotter, H Schmidt, M Schuur, PW Schofield, RJ Scott, VM Steen, DJ Stott, JC van Swieten, KD Taylor, J Trollor, S Trompet, AG Uitterlinden, G Weinstein, E Widen, BG Windham, JW Jukema, AF Wright, MJ Wright, Q Yang, H Amieva, JR Attia, DA Bennett, H Brodaty, AJ de Craen, C Hayward, MA Ikram, U Lindenberger, LG Nilsson, DJ Porteous, K Räikkönen, I Reinvang, I Rudan, PS Sachdev, R Schmidt, PR Schofield, V Srikanth, JM Starr, ST Turner, DR Weir, JF Wilson, C van Duijn, L Launer, AL Fitzpatrick, S Seshadri, TH Mosley, IJ Deary

TITLE:

Genetic contributions to variation in general cognitive function: a meta-analysis of genome-wide association studies in the CHARGE consortium (N=53949).

JOURNAL:

Molecular psychiatry Feb 2015, Vol 20, pp. 183-92

ABSTRACT:

General cognitive function is substantially heritable across the human life course from adolescence to old age. We investigated the genetic contribution to variation in this important, health- and well-being-related trait in middle-aged and older adults. We conducted a meta-analysis of genome-wide association studies of 31 cohorts (N=53,949) in which the participants had undertaken multiple, diverse cognitive tests. A general cognitive function phenotype was tested for, and created in each cohort by principal component analysis. We report 13 genome-wide significant single-nucleotide polymorphism (SNP) associations in three genomic regions, 6q16.1, 14q12 and 19q13.32 (best SNP and closest gene, respectively: rs10457441, P=3.93 × 10(-9), MIR2113; rs17522122, P=2.55 × 10(-8), AKAP6; rs10119, P=5.67 × 10(-9), APOE/TOMM40). We report one gene-based significant association with the HMGN1 gene located on chromosome 21 (P=1 × 10(-6)). These genes have previously been associated with neuropsychiatric phenotypes. Meta-analysis results are consistent with a polygenic model of inheritance. To estimate SNP-based heritability, the genome-wide complex trait analysis procedure was applied to two large cohorts, the Atherosclerosis Risk in Communities Study (N=6617) and the Health and Retirement Study (N=5976). The proportion of phenotypic variation accounted for by all genotyped common SNPs was 29% (s.e.=5%) and 28% (s.e.=7%), respectively. Using polygenic prediction analysis, ~1.2% of the variance in general cognitive function was predicted in the Generation Scotland cohort (N=5487; P=1.5 × 10(-17)). In hypothesis-driven tests, there was significant association between general cognitive function and four genes previously associated with Alzheimer's disease: TOMM40, APOE, ABCG1 and MEF2C. PUBMED: 25644384
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