脑源性神经营养因子在阿尔茨海默病中的作用

Effect of brain derived neurotrophic factor in Alzheimer disease

脑源性神经营养因子(BDNF)是神经营养因子家族(NTFs)的一员,能够促进神经元的存活及生长发育,能防止神经元受损死亡,对外周和中枢神经有保护作用,对抗β淀粉样蛋白沉积所致的神经毒性作用及细胞凋亡,可诱发及维持突触前及突触后的长时程增强效应(LTP),参与海马依赖的学习记忆过程。阿尔茨海默病(AD)是一种以记忆、人格、学习、认知功能改变为主要特征的神经系统退行性的疾病,是老年人痴呆中最常见的一种类型。自十余年前研究发现患者脑内BDNF的减少,推动了BDNF在AD患者中发病机制的研究。近几年研究发现在AD患者海马和皮质内BDNF mRNA的表达及蛋白含量均有所下降,表明BDNF水平与AD的发生发展有关,其与AD的关系已得到广泛重视。在AD的发病及发展过程中,外源性的BDNF可以保护神经元的完整性和功能,减少β淀粉样蛋白沉积对神经元的毒性作用,促进其特异性受体酪氨酸激酶B(TrkB)蛋白表达增强,促进内源性BDNF表达增强,进而对神经元起到保护作用,调节突触传递易化LTP,改善患者的学习记忆能力。

Brain derived neurotrophic factor （BDNF）, a member of the neurotrophic family of proteins, plays crucial roles in protecting the peripheral and central nervous systems. BDNF promotes the growth, development and survival of neurons, prevents neurons damage to death, fights against the neurotoxicity and apoptosis caused by beta amyloid deposition, induces or maintains the presynaptic and postsynaptic long-term potentiation （LTP）, and also participates in the process of hippocampus-dependent learning and memory. Alzheimer disease （AD） is a progressive neurodegenerative disorder that is characterized by cognitive decline with a progressive impairment of memory, personality and learning. It＇s the most common type of dementia. A great effort has been directed to the understanding of the effect of BDNF in the pathogcnesis of AD since a decline of BDNF level in the brains of AD patients were reported a decade ago. In recent years, emerging findings have revealed a decline in BDNF mRNA and protein expression in the hippocampus and cerebral cortex of AD patients, showed that BDNF level is related to the occurrence and development of AD, the relationship between BDNF and AD has received extensive attention. In the occurrence and development of AD, the exogenous BDNF can protect the integrity and the function of neurons, reduce the toxicity of plaque deposition, enhance the expression of its specific receptor tropomyosin-related kinase receptor type B （TrkB）, then enhance the expression of endogenous BDNF, therefore exert a protective role in neurons, mediate synaptic transmission and facilitate LTP, help to improve the learning and memory ability of AD patients.