memory, and executive functioning presenting in a trait-like manner (persisting during periods of euthymia). Data derived from family studies have clearly demonstrated heritability of cognitive impair- ment in families with a history of SZ and early evidence suggests a similar genetic influence in BPD. Thus, efforts to understand the underlying pathophysiology of neurocognitive impairment in BPD and SZ have necessarily begun to address the potential contributions of genetic variation to this trait across diagnostic categories. Recent data from candidate gene studies along with evidence from large- scale genome-wide investigations have led to the conclusion that there are likely to be some genes that impart a more generalized effect on susceptibility to psychopathology regardless of diagnosis (shared) and other genes with more illness-specific effects (unique). Likewise, insomuch as neurocognitive deficits reflect biomarkers related to risk for the illness, it follows that impairments common to both disorders are likely to be associated with shared genetic factors, while others may be more specific to either schizophrenia or bipolar disorder, based on phenotypic profiles. This presentation will first briefly describe the pattern and extent of cognitive impairment in BPD in contrast with SZ, with a focus on the influence of the overlapping feature of psychosis. Next, the neurocognitive deficits that appear to be most closely associated with genetic predisposition will be discussed, reviewing evidence of cosegregation in SZ families and providing new data derived from an ongoing discordant sibling pair study in BPD. Finally, several examples of candidate genes will be presented (e.g. DTNBP1; COMT) that have been consistently shown to influence neurocognition both within psychiatric samples and across the normal cognitive range. Concluding remarks will focus on the importance of utilizing intermediate phenotypes related to brain function to better understand the etiology of these complex diseases. doi:10.1016/j.schres.2010.02.079 Symposium 13 PHARMACOGENOMICS IN SCHIZOPHRENIA: HOW FAR TO THE CLINIC? Co-Chairpersons: Anil K. Malhotra, Alessandro Bertolino Monday,12 April, 2010 - 3:30 pm - 5:30 pm Overall Abstract: Recent research indicates that pharmacogenomic studies of antipsychotic drug response may be informative and there are now commercially available products to test specific genetic markers putatively associated with drug response. Nevertheless, the heterogeneity of drug response provides unique challenges for pharmacogenetics that may require novel approaches to fully realize the prospects for this area of inquiry. In this symposium, we will assess the status of pharmacogenomic testing in schizophrenia, with a focus on the acceptance and development of new approaches towards pharmacogenomic testing. Todd Lencz (New York, USA) will first discuss methodological issues in pharmacogenetics research including new developments in the assessment of complex pheno- types such as homozygosity mapping, rare variant detection, and the use of alternative in vitro and in vivo methods to identify candidate genes and candidate variants for examination. Alessandro Serretti (Bologna, Italy) will present data from an ongoing study of antipsychotic drug response, in which multiple genes underwent a detailed pharmacogenetic analysis with the aim of developing a complex predictive model to be used in everyday clinical practice. Alessandro Bertolino (Bari, Italy) will expand the discussion to incorporate the use of alternative endpoints, or endophenotypes, in pharmacogenomic studies. He will review data from his lab utilizing functional brain imaging and neurocognitive measures as response parameters in an olanzapine treatment study, as these phenotypes may more closely reflect the subtle effects of genetic variation on the brain. Anil Malhotra (New York, USA) will review data on the use of adverse events as a phenotype in pharmacogenomic studies, as side effects may be a more readily quantifiable dependent measure and perhaps be more critical to establishing treatment success than simple efficacy in schizophrenia. He will also discuss the develop- ment of commercial tests on the pharmacogenomics of adverse events, and address the strengths and weaknesses of this develop- ment. Finally, James Kennedy (Toronto, Canada) will serve as discussant and highlight areas of confluence and discrepancy from the various perspectives presented during the symposium, in order to fully synthesize the wealth of data in this rapidly emerging field. doi:10.1016/j.schres.2010.02.080 ISSUES REGARDING GENETIC TESTING FOR SCHIZOPHRENIA RISK AND FOR ANTIPSYCHOTIC DRUG EFFECTS James Kennedy, Matthew Lanktree, Gwyneth Zai, Jessica Sturgess, Daniel J. Mueller Centre for Addiction and Mental Health Toronto, ON, Canada The usefulness of genetic testing for schizophrenia (SCZ) is controversial. Proponents state that there is little else, besides family history, that provides any prediction of risk for schizophrenia, and some prediction is better than none. Furthermore, individuals should have the personal autonomy to choose whether to have the tests or not. The critics state that tests are not yet informative enough and may lead to premature / incorrect conclusions, and the educational tasks for clinicians and consumers to understand test results may be formidable. In the case of antipsychotic drug response, and in particular for side effects, there is likely a much clearer case to incorporate genetic testing into clinical practice. Methods: We surveyed 900 undergraduate and medical students with a 40 item questionnaire regarding opinions toward psychiatric genetic testing. Secondly, we genotyped 32 SCZ patients and 43 OCD patients from our CAMH hospital and retrospectively assessed medication response and side effects. Thirdly, we have introduced CYP450 gene testing as a prospective tool for choice of medication type and dosage, primarily directed at patients who are having difficulties with antipsychotic treatment. Results: In the student survey, there was strong support for the usefulness of pharmacogenetic tests, with 92% endorsement. In the scenario of testing for Huntingtons Disease, only 47% stated that they would have the test done on themselves if they were at risk, and 43% would refuse to have the test. For a genetic test for depression that would denote 'higher' vs 'lower' risk, 34% of respondents would agree to have such a test, and 54% would not. In the retrospective study of CYP2D6 genotype, we found significant correlation between poor or rapid metabolizer status and poor outcome in medication treatment. Our effort in prospective pharmacogenetic testing has yielded interesting case studies revealing a potential role for CYP450 gene tests in general clinical practice. Conclusions: Genetic testing for the diagnosis of SCZ does not appear useful at the present time. The risks of providing pharmacogenetic tests to physicians for their patients appear to be relatively low, and the early indications are that these kind of tests would be widely accepted. Limitations in terms of ethics, funding, and education will be discussed. doi:10.1016/j.schres.2010.02.081 Abstracts 129