Shared neurocognitive dysfunctions in young offspring at extreme risk for schizophrenia or bipolar disorder in eastern quebec multigenerational families.

Publication Type:

Journal Article


Schizophr Bull, Volume 35, Issue 5, p.919-30 (2009)


Adolescent, Bipolar Disorder, Cognition Disorders, Diagnostic and Statistical Manual of Mental Disorders, Early Diagnosis, Female, Genetic Predisposition to Disease, Genotype, Humans, Intelligence, Male, Neuropsychological Tests, Phenotype, Psychometrics, Quebec, Risk Assessment, Risk Factors, Schizophrenia, Schizophrenic Psychology, Young Adult


<p><b>BACKGROUND: </b>Adult patients having schizophrenia (SZ) or bipolar disorder (BP) may have in common neurocognitive deficits. Former evidence suggests impairments in several neuropsychological functions in young offspring at genetic risk for SZ or BP. Moreover, a dose-response relation may exist between the degree of familial loading and cognitive impairments. This study examines the cognitive functioning of high-risk (HR) offspring of parents having schizophrenia (HRSZ) and high-risk offspring of parents having bipolar disorder (HRBP) descending from densely affected kindreds.</p><p><b>METHODS: </b>The sample consisted of 45 young offspring (mean age of 17.3 years) born to a parent having SZ or BP descending from large multigenerational families of Eastern Québec that are densely affected by SZ or BP and followed up since 1989. The offspring were administered a lifetime best-estimate diagnostic procedure (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition [DSM-IV]) and an extensive standard neuropsychological battery. Raw scores were compared with age- and gender-matched controls.</p><p><b>RESULTS: </b>The offspring displayed differences in memory and executive functions when compared with controls. Moderate to large effect sizes (Cohen d) ranging from 0.65 to 1.25 (for IQ and memory) were observed. Several of the cognitive dysfunctions were present in both HRSZ and HRBP, even when considering DSM-IV clinical status.</p><p><b>CONCLUSIONS: </b>HRSZ and HRBP shared several aspects of their cognitive impairment. Our data suggest that the extremely high genetic and familial loading of these HRs may have contributed to a quantitatively increased magnitude of the cognitive impairments in both HR subgroups, especially in memory. These offspring at heightened risk present difficulties in processing information that warrant preventive research.</p>

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