老年焦虑症GABA能神经可塑性障碍及BDNF的潜在治疗作用  

The potential therapeutic effect of BDNF on GABAergic neuroplasticity dysfunction in late-life anxiety

作　　者：石安华[1] 孙晓菲[1] 周宁娜[1] 

机构地区：[1]云南中医学院基础医学院药理教研室,昆明650500

出　　处：《中华行为医学与脑科学杂志》2016年第6期572-576,共5页Chinese Journal of Behavioral Medicine and Brain Science

基　　金：国家自然科学基金（81260649）

摘　　要：老年焦虑症发病率高,且常与心脑血管疾病并存,使致残率和死亡率增加.其病理基础不同于成年人,脑内γ-氨基丁酸（γ-amino-butyric acid,GABA）能神经可塑性障碍是老年焦虑症的重要发病机制之一.目前临床治疗老年焦虑症的药物只能减轻焦虑症状,但不能改善神经功能,因而疗效欠佳.脑源性神经营养因子（Brain derived neurotrophic factor,BDNF）是介导脑内GABA能神经可塑性的重要信号分子,老年时期脑内BDNF不足可导致GABA能神经可塑性障碍而诱发焦虑行为.因此,通过增加脑内BDNF水平恢复GABA能神经可塑性是预防和治疗老年焦虑症的重要潜在靶点.Late-life anxiety has a high prevalence and usually co-morbidity with cerebral-and cardiovascular diseases which in turn increases the disability and mortality in old people.The pathology of late-life anxiety is difference from adult with the character of GABAergic neuroplasticity dysfunction.The therapeutic strategy presently can only alleviate the anxious symptom but not ameliorate the neuroplasticity.Brain-derived neurotrophic factor （BDNF） is a critical signaling molecule which regulates the GABAergic neuroplasticity,reduction of BDNF along with aging can induce GABAergic dysfunction which contributes to late-life anxiety.BDNF may exert anxiolytic effects by restoring the GABAergic plasticity and can be a potential therapeutic strategy of late-life anxiety.

关 键 词：老年焦虑症 神经可塑性障碍 神经营养机制 GABA BDNF 

分 类 号：R749.72[医药卫生—神经病学与精神病学]