Inflammation and Depression: Why Poststroke Depression may be the Norm and Not the Exception
Inflammation and Depression: Why Poststroke Depression may be the Norm and Not the Exception
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DOI：
10.1111/j.1747-4949.2010.00565.x
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发表时间：
2011-01
影响因子：
6.7
通讯作者：
M. Pascoe;S. Crewther;L. Carey;D. Crewther
中科院分区：
文献类型：
--
作者：
M. Pascoe;S. Crewther;L. Carey;D. Crewther
缺血性卒中常先于临床抑郁症的出现。卒中后抑郁反过来影响预后。为了促进我们对卒中后抑郁症发展的生物学机制的理解，本系统综述探讨了驱动情绪相关脑区炎症相关细胞死亡发展的免疫学过程。特别关注的是精氨酸驱动的内在凋亡因子，包括细胞内钙，谷氨酸兴奋毒性和自由基，出现在脑缺血损伤后，其存在显着增加临床定义的抑郁症的可能性。
Ischaemic stroke often precedes the appearance of clinical depression. Poststroke depression in turn influences the prognostic outcome. In the interest of advancing our understanding of the biological mechanisms underlying the development of poststroke depression, this systematic review explores the immunological processes driving the development of inflammation-related cell death in mood-related brain regions. Particular attention has been paid to cytokine-driven intrinsic apoptosis factors, including intracellular calcium, glutamate excitotoxicity and free radicals that appear in the brain following ischaemic damage and whose presence significantly increases the likelihood of clinically defined depression.