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Decreased serum neurotrophin 3 in chronically medicated schizophrenic males.

机译:慢性药物治疗的精神分裂症男性的血清神经营养蛋白3减少。

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摘要

There is evidence that major psychiatric disorders such as schizophrenia (SZ) are associated with deregulation of synaptic plasticity with downstream alterations of neurotrophins. NT3 is an important neurotrophin in the central nervous system, and performs key biological functions, such as promoting the survival, differentiation, and plasticity of neurons. NT3 has a central role in the early neuronal development; enhancing the survival of dopaminergic neurons, suggesting possible involvement in the physiopathology of dopamine related neuropsychiatric disorders such as SZ. Variations in the NT3 gene increase the risk of SZ. Three groups of chronically medicated DSM-IV patients with SZ, on treatment with clozapine (n=12), haloperidol (n=12), risperidone (n=12) and 10 healthy controls had 5ml blood samples collected by venipuncture. NT3 serum levels were assessed using sandwich-ELISA and were significantly lower in SZ patients (p0.005) when compared to either controls. These findings suggest that the NT3 signaling system may play a role in the pathophysiology of SZ and might be related to the course of illness or to treatment variables. Longitudinal studies are warranted.
机译:有证据表明,诸如精神分裂症(SZ)的主要精神疾病与神经营养蛋白下游改变引起的突触可塑性调节失调有关。 NT3是中枢神经系统中重要的神经营养蛋白,具有重要的生物学功能,如促进神经元的存活,分化和可塑性。 NT3在早期神经元发育中起着核心作用。增强多巴胺能神经元的存活,提示可能参与多巴胺相关神经精神疾病(例如SZ)的生理病理。 NT3基因的变异会增加患SZ的风险。三组慢性药物治疗的DSM-IV SZ患者,接受氯氮平(n = 12),氟哌啶醇(n = 12),利培酮(n = 12)和10名健康对照治疗,通过静脉穿刺收集5ml血液样本。 NT3血清水平通过三明治ELISA评估,与任一对照组相比,SZ患者的NT3血清水平显着降低(p <0.005)。这些发现表明NT3信号传导系统可能在SZ的病理生理中起作用,并且可能与疾病进程或治疗变量有关。纵向研究是必要的。

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