神经营养因子假说与抑郁症发病机制的研究进展

目前关于抑郁症发病机制的神经营养因子假说研究尚不明确,当前研究多聚焦于脑源性神经营养因子(BDNF)及其前体(proBDNF)和成熟体(mBDNF)在抑郁症中的作用。多个研究显示抑郁症患者proBDNF蛋白水平升高,而mBDNF蛋白水平降低。随着对神经营养因子假说研究的深入,有研究发现组织型纤溶酶原激活剂(tPA)可通过促使proBDNF向mBDNF转化而缓解抑郁症状,纤溶酶原激活物抑制剂-1(PAI-1)可抑制tPA的表达,PAI-1在抑郁症患者中的表达增加。本文对BDNF、proBDNF、mBDNF、tPA及PAI-1与抑郁症之间的关系进行综述,以期为抑郁症的发生机制及诊疗提供参考。

Research progress on neurotrophic factor hypothesis and the pathogenesis of depressive disorder

So far, the researches on the neurotrophic factor hypothesis of the pathogenesis of depression is not clear. Current research focuses more on the role of Brain - derived Neurotrophic Factor ( BDNF) and its precursor ( proBDNF) as well as maturation ( mBDNF) in depressive disorder. The researches indicate that the level of proBDNF protein increased while mBDNF protein level decreased in patients with depression. With deepening of the researches on neurotrophic factor hypothesis, it has been found that the tissue - type Plasminogen Activator ( tPA) can alleviate the symptoms of depression by promoting the translation of proBDNF into mBDNF, the Plasminogen Activator Inhibitor - 1 ( PAI - 1 ) can inhibit the expression of tPA, the expression of PAI - 1 in patients with depression increased. In this article, the relationship among BDNF, proBDNF, mBDNF, tPA and PAI - 1 with depression were reviewed, so as to provide references for the pathogenesis, diagnosis and treatment of depressive disorder.