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Heritability and molecular genetic basis of antisaccade eye tracking error rate: A genome‐wide association study
Author(s) -
Vaidyanathan Uma,
Malone Stephen M.,
Donnelly Jennifer M.,
Hammer Micah A.,
Miller Michael B.,
McGue Matt,
Iacono William G.
Publication year - 2014
Publication title -
psychophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.661
H-Index - 156
eISSN - 1469-8986
pISSN - 0048-5772
DOI - 10.1111/psyp.12347
Subject(s) - antisaccade task , heritability , endophenotype , psychology , genome wide association study , additive genetic effects , genetic association , genetics , single nucleotide polymorphism , biology , eye movement , gene , cognition , psychiatry , neuroscience , genotype , saccade
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.