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Antisaccade performance in schizophrenia patients, their first‐degree biological relatives, and community comparison subjects: Data from the COGS study
Author(s) -
Radant Allen D.,
Dobie Dorcas J.,
Calkins Monica E.,
Olincy Ann,
Braff David L.,
Cadenhead Kristin S.,
Freedman Robert,
Green Michael F.,
Greenwood Tiffany A.,
Gur Raquel E.,
Gur Ruben C.,
Light Gregory A.,
Meichle Sean P.,
Millard Steve P.,
Mintz Jim,
Nuechterlein Keith H.,
Schork Nicholas J.,
Seidman Larry J.,
Siever Larry J.,
Silverman Jeremy M.,
Stone William S.,
Swerdlow Neal R.,
Tsuang Ming T.,
Turetsky Bruce I.,
Tsuang Debby W.
Publication year - 2010
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/j.1469-8986.2010.01004.x
Subject(s) - endophenotype , antisaccade task , psychology , schizophrenia (object oriented programming) , first degree relatives , heritability , cognition , psychosis , clinical psychology , developmental psychology , psychiatry , family history , genetics , eye movement , saccade , neuroscience , medicine , biology
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.