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2014 ; 51
(12
): 1272-84
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Heritability and molecular genetic basis of antisaccade eye tracking error rate:
a genome-wide association study
#MMPMID25387707
Vaidyanathan U
; Malone SM
; Donnelly JM
; Hammer MA
; Miller MB
; McGue M
; Iacono WG
Psychophysiology
2014[Dec]; 51
(12
): 1272-84
PMID25387707
show ga
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.