This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Wealth of evidence suggests that schizophrenia is a genetic illness and the genotype is expressed as liability to illness. Schizotypal and related personalities and smooth pursuit eye movement (SPEM) abnormalities are highly prevalent in non-ill relatives of schizophrenic patients and mark the genetic liability to schizophrenia. Our proposal is based on the premise that in the presence of the genetic vulnerability, other non-genotypic factors lead to the overt expression of the illness. Non-genotypic factors are likely to be either environmental stress during development or non specific genetic factors critical for normal brain development. The broad goals of the protocol are: (1) Refine methods of examining eye movements in order to define the cognitive and ocular motor processes which mark the genetic liability; (2) Describe clinical and cognitive correlates of eye movement abnormality in vulnerable individuals; (3) Describe putative markers of non-genotypic factors which may have contributed to the development of the illness in the proband; and, (4) Conduct formal genetic linkage analysis using smooth pursuit eye movement abnormality as a phenotype. One of the goals of this study is to examine potential prenatal stress factors that may play a role in the etiology of schizophrenia. We hypothesize that within a family, individuals with and without the genetic liability, have equal probability of being exposed to putative stress factors. Of the genetically vulnerable individuals, those who are exposed to the stress will develop overt illness, whereas vulnerable individuals not exposed to the stress will only carry the phenotypic marker.
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