The common inflammatory etiology of depression and cognitive impairment: a therapeutic target

被引:199
作者
Allison, David J. [1 ]
Ditor, David S. [1 ]
机构
[1] Brock Univ, Fac Appl Hlth Sci, Dept Kinesiol, St Catharines, ON L2S 3A1, Canada
关键词
Indoleamine 2,3-dioxygenase; Tryptophan 2,3-dioxygenase; Kynurenine pathway; Chronic Inflammation; Depression; Cognitive impairment; Exercise; TUMOR-NECROSIS-FACTOR; ENDOGENOUS KYNURENIC ACID; C-REACTIVE PROTEIN; TO-BRAIN COMMUNICATION; ACUTE-PHASE RESPONSE; PHYSICAL-ACTIVITY; TRYPTOPHAN 2,3-DIOXYGENASE; HIPPOCAMPAL VOLUME; MAJOR DEPRESSION; QUINOLINIC ACID;
D O I
10.1186/s12974-014-0151-1
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
071005 [微生物学]; 100108 [医学免疫学];
摘要
Chronic inflammation has been shown to contribute to the development of a wide variety of disorders by means of a number of proposed mechanisms. Depression and cognitive impairment are two such disorders which may share a closely linked inflammatory etiology. The ability of inflammatory mediators to alter the activity of enzymes, from key metabolic pathways, may help explain the connection between these disorders. The chronic up-regulation of the kynurenine pathway results in an imbalance in critical neuroactive compounds involving the reduction of tryptophan and elevation of tryptophan metabolites. Such imbalances have established implications in both depression and cognitive impairment. This may implicate the immune system as a potential therapeutic target in the treatment of these disorders. The most common treatment modalities currently utilized, involve drug interventions which act on downstream targets. Such treatments help to reestablish protein balances, but fail to treat the inflammatory basis of the disorder. The use of anti-inflammatory interventions, such as regular exercise, may therefore, contribute to the effectiveness of current drug interventions in the treatment of both depression and cognitive impairment.
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页数:12
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