Neural correlates of antisaccade and delayed response task performance in participants with schizophrenia and their biological relatives
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Schizophrenia is characterized by problems with inhibition and working memory. For example, people with schizophrenia show abnormalities on antisaccade (AS) and ocular motor delayed response (ODR) tasks. Some of the first degree biological relatives of schizophrenia patients have similar abnormalities. The present study used fMRI with simultaneous eye movement recording to evaluate BOLD signal associated with AS and ODR task performance in three groups: schizophrenia patients, their biological relatives, and normal participants. Analyses revealed the following. First, behavioral results showed that (a) the schizophrenia patients generated significantly more errors than the normal group and (b) the relatives of schizophrenia patients showed intermediate error values which were only significantly different from the normal participants. Second, all subjects showed saccade-related activity in expected basal ganglia-thalamocortical circuitry mediating (a) saccade generation including striatum, lateral frontal eye fields (lFEF), supplementary eye fields (SEF), superior parietal lobule (SPL), cuneus and middle occipital gyrus (MOG), and (b) executive functioning including BA 9 and BA 10 in dorsolateral prefrontal cortex (DLPFC), anterior cingulate (ACG), medial FEF, and insula. Third, while schizophrenia patients and their relatives showed disruptions in BA 10, ACG, cuneus, MOG and insula, such disruptions observed in the relative group were intermediate. Fourth, schizophrenia patients showed additional disruptions in lFEF and SEF. In sum, the results suggest that the neural substrates underlying poor AS or ODR task performance are disrupted in participants with schizophrenia and their relatives. Results suggest that poor inhibition and working memory performance and its underlying neural substrates may be biological markers of schizophrenia.