| Literature DB >> 20374545 |
Allen D Radant1, Dorcas J Dobie, Monica E Calkins, Ann Olincy, David L Braff, Kristin S Cadenhead, Robert Freedman, Michael F Green, Tiffany A Greenwood, Raquel E Gur, Ruben C Gur, Gregory A Light, Sean P Meichle, Steve P Millard, Jim Mintz, Keith H Nuechterlein, Nicholas J Schork, Larry J Seidman, Larry J Siever, Jeremy M Silverman, William S Stone, Neal R Swerdlow, Ming T Tsuang, Bruce I Turetsky, Debby W Tsuang.
Abstract
The antisaccade task is a widely used technique to measure failure of inhibition, an important cause of cognitive and clinical abnormalities found in schizophrenia. Although antisaccade performance, which reflects the ability to inhibit prepotent responses, is a putative schizophrenia endophenotype, researchers have not consistently reported the expected differences between first-degree relatives and comparison groups. Schizophrenia participants (n=219) from the large Consortium on the Genetics of Schizophrenia (COGS) sample (n=1078) demonstrated significant deficits on an overlap version of the antisaccade task compared to their first-degree relatives (n=443) and community comparison subjects (CCS; n=416). Although mean antisaccade performance of first-degree relatives was intermediate between schizophrenia participants and CCS, a linear mixed-effects model adjusting for group, site, age, and gender found no significant performance differences between the first-degree relatives and CCS. However, admixture analyses showed that two components best explained the distributions in all three groups, suggesting two distinct doses of an etiological factor. Given the significant heritability of antisaccade performance, the effects of a genetic polymorphism is one possible explanation of our results.Entities:
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Year: 2010 PMID: 20374545 PMCID: PMC4176871 DOI: 10.1111/j.1469-8986.2010.01004.x
Source DB: PubMed Journal: Psychophysiology ISSN: 0048-5772 Impact factor: 4.016