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炎症与抑郁:为何卒中后抑郁可能是常态而非例外

Inflammation and depression: why poststroke depression may be the norm and not the exception.

机构信息

Brain Sciences Institute, Swinburne University, Melbourne, Vic, Australia.

出版信息

Int J Stroke. 2011 Apr;6(2):128-35. doi: 10.1111/j.1747-4949.2010.00565.x. Epub 2011 Jan 19.

DOI:10.1111/j.1747-4949.2010.00565.x
PMID:21371275
Abstract

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.

摘要

缺血性中风通常先于临床抑郁症出现。反过来,中风后抑郁症又会影响预后结果。为了深入了解导致中风后抑郁症发展的生物学机制,本系统综述探讨了驱动与情绪相关的大脑区域中炎症相关细胞死亡的免疫过程。特别关注了细胞因子驱动的内在凋亡因子,包括细胞内钙、谷氨酸兴奋性毒性和自由基,这些物质在缺血性损伤后出现在大脑中,其存在显著增加了临床定义的抑郁症的可能性。

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