Here we report results from a GWAS of intelligence in middle to older adulthood. Despite the fact that no specific genetic variants have been robustly associated with human intelligence, apart perhaps for APOE at older ages34,35, our results show for the first time that a substantial proportion (approximately 40 to 50%) of variation in human intelligence is associated with common SNPs (Minor allele frequency (MAF) > 0.01) that are in LD with causal variants. These results are consistent with a highly polygenic model because we detect variation across the entire genome. If the narrow-sense heritability for intelligence is approximately 0.6 in the age groups studied in the CAGES samples3,36, then not all additive variation is accounted for by our analyses. One reason for this difference could be that causal variants for intelligence have, on average, a lower MAF than the SNPs on the chip used. Such a frequency difference causes imperfect LD between the genotyped SNPs and unobserved causal variants. Traditional pedigree analysis is not affected by such imperfect LD because it is based on the correct expected identity-by-descent coefficients
