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.
Original language | English |
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Pages (from-to) | 47-52 |
Number of pages | 6 |
Journal | Schizophrenia Research |
Volume | 163 |
Issue number | 1-3 |
DOIs | |
State | Published - 1 Apr 2015 |
Externally published | Yes |
Bibliographical note
Publisher Copyright:© 2014.
Funding
Dr. Green has been a consultant to AbbVie, Biogen, DSP, EnVivo/Forum and Roche, and he is on the scientific advisory board of Mnemosyne. He has received research funds from Amgen. Dr. Lazzeroni is an inventor on a patent application filed by Stanford University on genetic polymorphisms associated with depression. Dr. Light has been a consultant to EnVivo/Forum and Astellas and serves on an advisory board for Neuroverse. Dr. Nuechterlein has received unrelated research support from Janssen Scientific Affairs, Genentech, and Brain Plasticity, Inc., and he has consulted for Genentech, Otsuka, Janssen, and Brain Plasticity, Inc. Dr. Swerdlow has been a consultant for Genco Sciences, Ltd. All other authors declare that they have no conflict of interest. This material is based upon work supported (or supported in part) by the Office of Research and Development Medical Research Service (or) Health Services R&D Service, Department of Veterans Affairs. This study was supported by NIMH grants R01 MH65571 , R01 MH65588 , R01 MH65562 , R01 MH65707 , R01 MH65554 , R01 MH65578 , and R01 MH65558 .
Funders | Funder number |
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Brain Plasticity, Inc. | |
Office of Research and Development Medical Research Service | |
Otsuka | |
National Institutes of Health | |
National Institute of Mental Health | R01 MH65558, R01MH086135, R01 MH65707, R01MH065562, R01 MH65571, R01 MH65578, R01 MH65588, R01 MH65554 |
U.S. Department of Veterans Affairs | |
Genentech | |
Janssen Pharmaceuticals | |
Janssen Scientific Affairs |
Keywords
- Antisaccade task
- Recruitment