Heritability and molecular genetic basis of antisaccade eye tracking error rate: a genome-wide association study.
Antisaccade deficits reflect abnormalities in executive function linked to various disorders including schizophrenia, externalizing psychopathology, and neurological conditions. We examined the genetic bases of antisaccade error in a sample of community-based twins and parents (N = 4,469). Biometric models showed that about half of the variance in the antisaccade response was due to genetic factors and half due to nonshared environmental factors. Molecular genetic analyses supported these results, showing that the heritability accounted for by common molecular genetic variants approximated biometric estimates. Genome-wide analyses revealed several SNPs as well as two genes-B3GNT7 and NCL-on Chromosome 2 associated with antisaccade error. SNPs and genes hypothesized to be associated with antisaccade error based on prior work, although generating some suggestive findings for MIR137, GRM8, and CACNG2, could not be confirmed.
Department of Psychology, University of Minnesota, Minneapolis, Minnesota, USA.
Uma
U
Vaidyanathan
Stephen M
SM
Malone
Jennifer M
JM
Donnelly
Micah A
MA
Hammer
Michael B
MB
Miller
Matt
M
McGue
William G
WG
Iacono
D000293:Adolescent; D000328:Adult; D000368:Aged; D058068:Endophenotypes; D055106:Genome-Wide Association Study; D006801:Humans; D008875:Middle Aged; D008969:Molecular Sequence Data; D009483:Neuropsychological Tests; D010290:Parents; D020641:Polymorphism, Single Nucleotide; D012438:Saccades / Q000235:genetics*; D014427:Twins / Q000235:genetics*
Antisaccade; Endophenotypes; GCTA; Gene-based tests; Genome-wide association study; Heritability; Molecular genetics