VEGF调控抑郁症海马神经发生的研究进展

VEGF Regulation of Hippocampal Neurogenesis in Depression

抑郁症是一种发生率高、易复发、危害大的精神障碍,其主要临床表现是持续的情绪低落和认知功能障碍。近年来其发病率越来越高,已经引起了人们广泛关注,由于其发病机制比较复杂,目前尚未完全阐明。神经营养假说认为,神经营养因子具有维持神经元生存、促进突触生长的作用,倘若前额叶、海马等脑区神经营养因子缺乏,可抑制相应脑功能从而最终导致抑郁;故抗抑郁药物治疗抑郁的途径是增加脑中的神经营养因子含量、提高突触可塑性和促进神经元生存。总之神经营养因子表达水平下降参与了抑郁症的病理生理过程。在众多神经营养因子中,VEGF是一种多功能的因子,能够通过多种途径促进血管生成,保护缺血和退变的神经元,引发成年大脑神经元再生,从而影响抑郁。而研究表明,成年海马神经发生与正在进行的血管生成是有着密切的联系。本文主要对VEGF在海马神经发生的作用机制及其调控对抑郁症的影响进行阐述。发现VEGF在调节海马神经发生具有重要的作用,并且VEGF及其下游信号参与了抑郁症的发生发展过程。

Depression is one of harmful mental disorders with a high prevalence and relapse rate. Persistent depression and cognitive dysfunction are its main clinical features. Recently an increasing incidence of depression is widely focused. However, due to its complication, pathological mechanism has not been fully elucidated yet. The neurotrophic hypothesis proposes that neurotrophic factors can promote the growth of synapse and maintain neurons survival. Ifneurotrophic factors is difficient in some certain brain areas such as the prefrontal cortex and the hippocampus, it may be the result of the inhibition of corresponding brain function, which may eventually lead to depression. Meanwhile the mechanism of antidepressant drugs is mainly to increase the brain neurotrophic factor levels and to improve synaptic plasticity and promote the survival of neurons to exert its effect of treatment. In other words, the decreased expression of neurotrophic factors is involved in the pathophysiological procedure in depression. VEGF, as a multifimctional factor among the various neurotrophic factors, an effectively promote angiogenesis and protect ischemic and degenerated neurons, regenerating neurons in the brain. Current studies have indicated that adult hippocampal neurogenesis and ongoing angiogenesis are closely connected. This paper rewiewed the role mechanism for VEGF in hippocampal neurogenesis and its regulation effect in depression and found that VEGF played an important role in the hippocampal neurogenesis regulation, and VEGF and its downstream signal were involved in the onset and maintainance of depression.