摘要
抑郁症(depression)是一种以情绪低落、悲观厌世、认知和睡眠障碍为主要特征的情感性精神障碍,临床一线抗抑郁药主要是基于单胺假说的药物,通过对单胺递质的调节发挥抗抑郁作用,尽管疗效肯定,但普遍存在起效延迟、有效率低、不良反应多等诸多缺憾,单胺假说也不能解释抑郁症的全部现象。因此,近年来除单胺假说外的其它假说越来越引起重视,炎症假说认为应激刺激引发炎症过程,最终导致抑郁症的发生,该文着重通过抑郁症的(神经)炎症假说阐述抑郁症与炎症的关系。
Depression is an affective disorder characterized by a state of low mood, pessimism, cognitive and sleep disorders. Despite the widespread prescription of monoaminergic neurotransmitter modulators, the monoamine hypothesis cannot explain all the phenomena of depression. Moreover, limited drug efficacies, slow onset of action and undesirable side effects have made urgent the task of discovering novel therapeutics. Thus, several hypotheses other than the monoamine hypothesis have received much attention in recent years. The inflammatory hypothesis of depression is that inflammatory mechanisms play a crucial role in the pathophysiological mechanisms of major depression. This review will focus on progress of the (neuro)inflammatory hypothesis of depression.
出处
《神经药理学报》
2013年第5期27-37,共11页
Acta Neuropharmacologica
基金
国家自然科学基金项目(No.81274122
No.81202507
No.81373997
No.81373998)
国家"重大新药创制"科技重大专项项目(No.2012ZX09301002-004
No.2012ZX09103101-006)
北京市自然科学基金项目(No.7142115
No.7131013)
教育部博士点基金重点项目(No.20121106130001)
新药作用机制研究与药效评价北京市重点实验室资助项目(No.BZ0150)
中央级公益性科研所基本科研业务费专项资金项目(No.2014RC03)
关键词
抑郁症
前炎症因子
抗抑郁药
抗炎药
发病机制
depression
proinflammatory cytokine
antidepressant
anti-inflammatory
pathogenesis