OBJECTIVE: Evidence suggests that poor eye tracking relates to genetically transmitted vulnerability for schizophrenia. The authors tested competing models for the genetic transmission of poor eye tracking in a search for major gene effects. METHOD: Samples from three studies (conducted in Minneapolis, New York, and Vancouver, B.C.) were pooled. Probands (N = 92) were diagnosed as schizophrenic by DSM-III criteria. Of the comparison subjects (N = 171), Vancouver patients were an epidemiologic first-episode group; at other sites unselected admitted patients were studied. First-degree relatives (N = 146) of 65 probands were also studied. Eye tracking was measured while subjects followed a horizontally moving, sinusoidally driven (0.4 Hz) spot of light on a screen. Performance was quantified by root mean square error. Data analysis was by complex segregation analysis (Bonney's class D regressive models). RESULTS: A single major gene is needed to account for poor eye tracking in schizophrenic patients and their relatives. This gene alone can explain about two-thirds of the variance in eye tracking performance. A single gene alone (regardless of dominance) will, however, not account for the data; polygenic factors are also required. CONCLUSIONS: Results support postulation of a single gene for ocular motor dysfunction, which may be a risk factor for schizophrenia. Eye tracking may be useful as a gene carrier test in genetic studies of schizophrenia.
OBJECTIVE: Evidence suggests that poor eye tracking relates to genetically transmitted vulnerability for schizophrenia. The authors tested competing models for the genetic transmission of poor eye tracking in a search for major gene effects. METHOD: Samples from three studies (conducted in Minneapolis, New York, and Vancouver, B.C.) were pooled. Probands (N = 92) were diagnosed as schizophrenic by DSM-III criteria. Of the comparison subjects (N = 171), Vancouver patients were an epidemiologic first-episode group; at other sites unselected admitted patients were studied. First-degree relatives (N = 146) of 65 probands were also studied. Eye tracking was measured while subjects followed a horizontally moving, sinusoidally driven (0.4 Hz) spot of light on a screen. Performance was quantified by root mean square error. Data analysis was by complex segregation analysis (Bonney's class D regressive models). RESULTS: A single major gene is needed to account for poor eye tracking in schizophrenicpatients and their relatives. This gene alone can explain about two-thirds of the variance in eye tracking performance. A single gene alone (regardless of dominance) will, however, not account for the data; polygenic factors are also required. CONCLUSIONS: Results support postulation of a single gene for ocular motor dysfunction, which may be a risk factor for schizophrenia. Eye tracking may be useful as a gene carrier test in genetic studies of schizophrenia.
Authors: L Elliot Hong; Kathleen A Turano; Hugh O'Neill; Lei Hao; Ikwunga Wonodi; Robert P McMahon; Amie Elliott; Gunvant K Thaker Journal: Biol Psychiatry Date: 2007-07-30 Impact factor: 13.382