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[重度抑郁症与脑源性神经营养因子(BDNF)]

[Major depressive disorders and BDNF (brain-derived neurotrophic factor)].

作者信息

Shimizu Eiji, Hashimoto Kenji, Iyo Masaomi

机构信息

Department of Psychiatry (K2), Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670 Japan.

出版信息

Nihon Shinkei Seishin Yakurigaku Zasshi. 2004 Jun;24(3):147-50.

Abstract

We reviewed the pre-clinical and clinical papers demonstrating that BDNF plays a role in the pathophysiology of major depressive disorders. Experimental studies suggest that BDNF expression is induced by chronic antidepressant treatments, and that BDNF itself have antidepressant activity in animal models of depression. Furthermore, BDNF may protect neurons against stress-induced damage, and affect neurogenesis in the adult hippocampus. Our clinical study showed that serum levels of BDNF in drug naive patients with depression were significantly decreased as compared with normal controls. These findings suggest that low BDNF levels may play a pivotal role in the pathophysiology of major depression. It is unclear whether low BDNF levels are primary or secondary in patients with depression. One hypothesis would be that reduced BDNF might reflect a genetic vulnerability in patients with depression. Another possible explanation would be that stress-induced BDNF reductions might cause neuronal damage, which would in turn lead to acquired biological vulnerability. In order to determine the precise mechanism underlying the relationship between reduced BDNF levels and the etiology of major depression under both genetic and environmental backgrounds, further detailed study will be necessary.

摘要

我们回顾了临床前和临床研究论文,这些论文表明脑源性神经营养因子(BDNF)在重度抑郁症的病理生理学中发挥作用。实验研究表明,慢性抗抑郁治疗可诱导BDNF表达,并且BDNF本身在抑郁症动物模型中具有抗抑郁活性。此外,BDNF可保护神经元免受应激诱导的损伤,并影响成年海马体中的神经发生。我们的临床研究表明,与正常对照组相比,未经药物治疗的抑郁症患者血清BDNF水平显著降低。这些发现表明,低BDNF水平可能在重度抑郁症的病理生理学中起关键作用。目前尚不清楚抑郁症患者中BDNF水平低是原发性还是继发性的。一种假设是,BDNF降低可能反映了抑郁症患者的遗传易感性。另一种可能的解释是,应激诱导的BDNF降低可能导致神经元损伤,进而导致获得性生物学易感性。为了确定在遗传和环境背景下BDNF水平降低与重度抑郁症病因之间关系的精确机制,有必要进行进一步的详细研究。

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