作者: Takanori Hashimoto , David A. Lewis
DOI: 10.1176/APPI.AJP.163.3.534
关键词: Neurotrophic factors 、 Prefrontal cortex 、 Schizophrenia 、 Gene expression 、 Neuroscience 、 Endocrinology 、 Psychology 、 Psychosis 、 Brain-derived neurotrophic factor 、 Tropomyosin receptor kinase B 、 Internal medicine 、 Glutamate decarboxylase
摘要: OBJECTIVE: In the prefrontal cortex of subjects with schizophrenia, decreased signaling mediated by brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase (TrkB) appears to contribute reduced expression mRNA encoding 67-kilodalton isoform glutamate decarboxylase (GAD67), an enzyme for GABA synthesis. The authors examined in schizophrenia effect human BDNF gene a single nucleotide polymorphism (Val66Met), which reduces trafficking secretion protein, on GAD67 mRNA. METHOD: Val66Met genotyping was performed 27 matched pairs comparison subjects. impact this assessed comparing within-pair differences between versus without Met66 allele after level controlled. RESULTS: contrast expectations, wit...