Heritability and molecular genetic basis of antisaccade eye tracking error rate: A genome-wide association study

Stephen M. Malone, Jennifer M. Donnelly, Micah A. Hammer, Michael B. Miller, Matt Mcgue, William G. Iacono

Research output: Contribution to journalArticlepeer-review

19 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1272-1284
Number of pages13
JournalPsychophysiology
Volume51
Issue number12
DOIs
StatePublished - Dec 1 2014

Bibliographical note

Publisher Copyright:
© 2014 Society for Psychophysiological Research.

Keywords

  • Antisaccade
  • Endophenotypes
  • GCTA
  • Gene-based tests
  • Genome-wide association study
  • Heritability
  • Molecular genetics

Fingerprint

Dive into the research topics of 'Heritability and molecular genetic basis of antisaccade eye tracking error rate: A genome-wide association study'. Together they form a unique fingerprint.

Cite this