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Войти в исследования International journal of methods in psychiatric research · 2018
Altered serum levels of glial cell line-derived neurotrophic factor in male chronic schizophrenia patients with tardive dyskinesia.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Ye Fei, Zhan Qiongqiong, Xiao Wenhuan, Sha Weiwei, Zhang Xiaobin
Аннотация
OBJECTIVES: Many research indicate that the tardive dyskinesia (TD) is generally linked with long-term antipsychotic therapy for schizophrenia. Glial cell line-derived neurotrophic factor (GDNF) is a critical role in the protection of catecholaminergic, dopaminergic, and cholinergic neurons. Thus, we examined the serum GDNF levels in schizophrenia patients with TD (WTD) and without TD (NTD) and compared with healthy controls (HC), respectively.
METHODS: Totally 75 males with schizophrenia were recruited into this study. All were measured by the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, the Positive and Negative Syndrome Scale, and the Abnormal Involuntary Movement Scale (AIMS). The patient group was divided into two subgroups: WTD (n = 32) and NTD (n = 43) according to the AIMS score. Fifty-three healthy controls matching in age and gender were also enlisted from the region. GDNF levels were examined with sandwich enzyme-linked immunosorbent assay.
RESULTS: Analysis of variance indicated significant differences between the three groups (P = 0.012); GDNF levels in the WTD group were significantly different from those in the NTD (P = 0.030) and HC (P = 0.003) groups.
CONCLUSION: Decreased GDNF levels in TD patients indicated that alterations in neurotrophic factors may be involved in the pathophysiology of TD, but the exact mechanisms need further investigation.
METHODS: Totally 75 males with schizophrenia were recruited into this study. All were measured by the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, the Positive and Negative Syndrome Scale, and the Abnormal Involuntary Movement Scale (AIMS). The patient group was divided into two subgroups: WTD (n = 32) and NTD (n = 43) according to the AIMS score. Fifty-three healthy controls matching in age and gender were also enlisted from the region. GDNF levels were examined with sandwich enzyme-linked immunosorbent assay.
RESULTS: Analysis of variance indicated significant differences between the three groups (P = 0.012); GDNF levels in the WTD group were significantly different from those in the NTD (P = 0.030) and HC (P = 0.003) groups.
CONCLUSION: Decreased GDNF levels in TD patients indicated that alterations in neurotrophic factors may be involved in the pathophysiology of TD, but the exact mechanisms need further investigation.