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

  • Author(s): Radant, AD
  • Millard, SP
  • Braff, DL
  • Calkins, ME
  • Dobie, DJ
  • Freedman, R
  • Green, MF
  • Greenwood, TA
  • Gur, RE
  • Gur, RC
  • Lazzeroni, LC
  • Light, GA
  • Meichle, SP
  • Nuechterlein, KH
  • Olincy, A
  • Seidman, LJ
  • Siever, LJ
  • Silverman, JM
  • Stone, WS
  • Swerdlow, NR
  • Sugar, CA
  • Tsuang, MT
  • Turetsky, BI
  • Tsuang, DW
  • et al.
Abstract

© 2014. 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.

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