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Schizophr Res. 2015 Apr;163(1-3):47-52. doi: 10.1016/j.schres.2014.12.016. Epub 2014 Dec 29.

Robust differences in antisaccade performance exist between COGS schizophrenia cases and controls regardless of recruitment strategies.

Author information

1
Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA, USA; Department of Veteran affairs (DVA), VISN-20, Mental Health Services, Seattle, WA, USA.
2
DVA, VISN-20, Mental Illness Research, Education, and Clinical Center (MIRECC), Seattle, WA, USA.
3
Department of Psychiatry, University of California, San Diego, San Diego, CA, USA; DVA, VISN-22 MIRECC, San Diego Healthcare System, San Diego, CA, USA.
4
Department of Psychiatry, University of Pennsylvania, Philadelphia, PA, USA.
5
Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA, USA; DVA, VISN-20, Mental Illness Research, Education, and Clinical Center (MIRECC), Seattle, WA, USA.
6
Department of Psychiatry, University of Colorado Health Sciences Center, Aurora, CO, USA.
7
Department of Psychiatry and Biobehavioral Sciences, Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA, USA.
8
Department of Psychiatry, University of California, San Diego, San Diego, CA, USA.
9
Department of Biostatistics, Stanford University, Palo Alto, CA, USA.
10
Massachusetts Mental Health Center, Public Psychiatry Division of the Beth Israel Deaconess Medical Center, Harvard Medical School, Department of Psychiatry, Harvard Institute of Psychiatric Epidemiology and Genetics, Boston, MA, USA.
11
Department of Psychiatry, Mount Sinai School of Medicine, New York, NY, USA; DVA, VISN-3, MIRECC, James J. Peters VA Medical Center, Bronx, NY, USA.
12
Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, WA, USA; DVA, VISN-20, Geriatric Research, Education, and Clinical Center, Seattle, WA, USA.

Abstract

The impaired ability to make correct antisaccades (i.e., antisaccade performance) is well documented among schizophrenia subjects, and researchers have successfully demonstrated that antisaccade performance is a valid schizophrenia endophenotype that is useful for genetic studies. However, it is unclear how the ascertainment biases that unavoidably result from recruitment differences in schizophrenia subjects identified in family versus case-control studies may influence patient-control differences in antisaccade performance. To assess the impact of ascertainment bias, researchers from the Consortium on the Genetics of Schizophrenia (COGS) compared antisaccade performance and antisaccade metrics (latency and gain) in schizophrenia and control subjects from COGS-1, a family-based schizophrenia study, to schizophrenia and control subjects from COGS-2, a corresponding case-control study. COGS-2 schizophrenia subjects were substantially older; had lower education status, worse psychosocial function, and more severe symptoms; and were three times more likely to be a member of a multiplex family than COGS-1 schizophrenia subjects. Despite these variations, which were likely the result of ascertainment differences (as described in the introduction to this special issue), the effect sizes of the control-schizophrenia differences in antisaccade performance were similar in both studies (Cohen's d effect size of 1.06 and 1.01 in COGS-1 and COGS-2, respectively). This suggests that, in addition to the robust, state-independent schizophrenia-related deficits described in endophenotype studies, group differences in antisaccade performance do not vary based on subject ascertainment and recruitment factors.

KEYWORDS:

Antisaccade task; Recruitment

PMID:
25553977
PMCID:
PMC4382408
DOI:
10.1016/j.schres.2014.12.016
[Indexed for MEDLINE]
Free PMC Article

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