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

被引：75

作者：

Pascoe, Michaela C. ^{[2
]}

Crewther, Sheila G. ^{[1
]}

Carey, Leeanne M. ^{[3
]}

Crewther, David P. ^{[2
]}

机构：

[1] La Trobe Univ, Sch Psychol Sci, Melbourne, Vic 3086, Australia

[2] Swinburne Univ Technol, Brain Sci Inst, Melbourne, Vic, Australia

[3] Florey Neurosci Inst, Natl Stroke Res Inst, Melbourne, Vic, Australia

来源：

INTERNATIONAL JOURNAL OF STROKE | 2011年 / 6卷 / 02期

关键词：

apoptosis; cytokine; depression; inflammation; ischaemia; NITRIC-OXIDE SYNTHASE; ISCHEMIC BRAIN-INJURY; NECROSIS-FACTOR-ALPHA; CEREBRAL-ARTERY OCCLUSION; KAPPA-B ACTIVATION; ACUTE MYOCARDIAL-INFARCTION; MESSENGER-RNA EXPRESSION; APOPTOTIC CELL-DEATH; SPINAL-CORD-INJURY; MAJOR DEPRESSION;

D O I：

10.1111/j.1747-4949.2010.00565.x

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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.

引用

页码：128 / 135

页数：8

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