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[抑郁症的神经营养假说]

[The neurotrophic hypothesis of depression].

作者信息

Bus B A A, Molendijk M L

出版信息

Tijdschr Psychiatr. 2016;58(3):215-22.

PMID:26979853
Abstract

BACKGROUND

The neurotrophic hypothesis of depression postulates that neuronal plasticity is a key factor in the development of depression and in the clinical response to antidepressants. Brain-derived neurotrophic factor (BDNF) is an important protein in this process.

AIM

To provide a survey of the current scientific view regarding the neurotrophic hypothesis of depression.

METHOD

We studied the literature using PubMed.

RESULTS

The serum bdnf level was found to be consistently lower in depressed patients compared to healthy controls. In short open-label antidepressant treatment trials the bdnf levels were found to be higher post-treatment than pre-treatment. Longitudinal analysis of a large naturalistic cohort study revealed that it was more likely that bdnf serum levels were lower as a result of depression than that they represented an etiological factor for the illness.

CONCLUSION

These findings show that the neurotrophic hypothesis of depression is more complex than previously assumed. Animal studies have shown a correlation between stress, diminished bdnf expression in the brain and depressive-like behavior. Studies in humans, on the other hand, particularly those with a longitudinal design, suggest that the decrease in serum bdnf is a consequence of the depression rather than vice versa. This is in sharp contrast to the original assumptions of the neurotrophic hypothesis.

摘要

背景

抑郁症的神经营养假说假定神经元可塑性是抑郁症发生及对抗抑郁药临床反应的关键因素。脑源性神经营养因子(BDNF)是这一过程中的一种重要蛋白质。

目的

对当前关于抑郁症神经营养假说的科学观点进行综述。

方法

我们使用PubMed检索文献。

结果

与健康对照相比,抑郁症患者血清BDNF水平持续较低。在短期开放标签抗抑郁治疗试验中,发现治疗后BDNF水平高于治疗前。一项大型自然队列研究的纵向分析显示,BDNF血清水平降低更可能是抑郁症的结果,而非该疾病的病因。

结论

这些发现表明,抑郁症的神经营养假说比之前设想的更为复杂。动物研究表明应激、大脑中BDNF表达减少与抑郁样行为之间存在关联。另一方面,人类研究,尤其是那些采用纵向设计的研究表明,血清BDNF降低是抑郁症的结果,而非相反。这与神经营养假说的最初设想形成鲜明对比。

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