期刊
SCHIZOPHRENIA RESEARCH
卷 89, 期 1-3, 页码 299-307出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.schres.2006.08.003
关键词
schizophrenia; early psychosis; prodromal; genetic high risk; clinical high risk; neurocognitive functioning
类别
资金
- NIMH NIH HHS [MH54186] Funding Source: Medline
- NATIONAL INSTITUTE OF MENTAL HEALTH [R01MH054186] Funding Source: NIH RePORTER
Objective: The purpose of the present study was to evaluate both the independent and joint effects of genetic risk and clinical status on neurocognitive functioning in adolescents from a population isolate with an elevated risk for schizophrenia and strong familial aggregation of cases. Method: The subjects were 3 10 non-help seeking, drug-naive adolescents 14-19 years of age from the Republic of Palau. The sample comprised 98 Genetically High Risk (GHR) adolescents, 54 of whom were symptomatic, and 212 Genetically Low Risk (GLR) adolescents, including 113 Clinically High Risk (CHR) subjects who were symptomatic and 99 normal controls who were non-symptomatic. Neurocognitive testing was conducted after the clinical assessment and included Wechsler Memory Scale tests of logical, visual and working memory, the perceptual organization and processing speed subtests of the WISC-III, CPT-IP measures of sustained attention, and tests of fine and gross neuromotor function. Results: GHR adolescents showed impairments in immediate logical memory, verbal working memory, CPT-IP performance, and fine motor skills. The only two cognitive components influenced by the presence of early psychosis symptoms were WISC-III perceptual organization and spatial working memory. Neurocognitive deficits did not increase with increasing levels of psychopathology. We found no significant interactive effects of genetic risk and clinical status on neurocognitive functioning. Conclusions: Genetic risk and clinical status exert independent effects on neurocognitive function in FIR adolescents, and genetic risk has a broader impact than clinical status. Our results suggest that many of the neurocognitive impairments associated with early psychosis are genetically mediated and can occur in genetically vulnerable individuals regardless of their clinical status. However, visuospatial processing appears to be uniquely disrupted by emerging symptomatology. (c) 2006 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据