期刊
NEUROSCIENCE AND BIOBEHAVIORAL REVIEWS
卷 51, 期 -, 页码 15-30出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neubiorev.2014.12.016
关键词
Brain-derived neurotrophic factor; BDNF; Val66Met; G196A; rs6265; Schizophrenia; Psychosis; Age of onset; Comorbid symptoms; Cognition; Therapeutic responsiveness; Brain morphology; Clinical pleiotropy; Animal models of schizophrenia; Val66Met mice
资金
- Australian Postgraduate Award (APA) from the University of Melbourne
- National Health & Medical Research Council (NHMRC) Career Development Fellowship
- NHMRC Senior Research Fellowship
Schizophrenia is believed to arise from complex gene environment interactions. Brain-derived neurotrophic factor (BDNF) is involved in neuronal development, differentiation and plasticity. A functional single nucleotide polymorphism that results in a valine (Val) to methionine (Met) substitution at codon 66 (Val66Met) results in the aberrant sorting and release of mature BDNF through the activity-dependent secretion pathway. The Val66Met polymorphism has been linked to impaired neurocognitive function in healthy adults, and identified as a locus of risk for a range of neuropsychiatric disorders including schizophrenia. Here we provide a comprehensive review of the relationship between the BDNF Val66Met polymorphism and schizophrenia, integrating evidence from the fields of genetic epidemiology, clinical psychiatry, behavioral neuroscience and neuroimaging. We argue that while the Val66Met polymorphism may not be a major risk-conferring agent for the development of schizophrenia per se, there is mounting evidence that the polymorphism modulates a range of clinical features of the illness, including age of onset, symptoms, therapeutic responsiveness, neurocognitive function and brain morphology. (C) 2015 Elsevier Ltd. All rights reserved.
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