SCI and depression: Does inflammation commandeer the brain?

被引:15
作者
Brakel, Kiralyn [1 ,2 ]
Hook, Michelle A. [1 ,2 ]
机构
[1] Texas A&M Univ, Dept Neurosci & Expt Therapeut, Sch Med, Med Res & Educ Bldg,Ste 1005,8447 Riverside Pkwy, College Stn, TX 77843 USA
[2] Texas A&M Univ, Texas A&M Inst Neurosci, Interdisciplinary Life Sci Bldg,Rm 3148, College Stn, TX USA
关键词
Depression; Spinal cord injury; Inflammation; HPA axis; SPINAL-CORD-INJURY; MIGRATION-INHIBITORY FACTOR; QUALITY-OF-LIFE; DOPAMINE TRANSPORTER BINDING; ELEVATED CIRCULATING LEVELS; ANXIETY-LIKE BEHAVIOR; FACTOR-KAPPA-B; MAJOR DEPRESSION; GUT MICROBIOTA; NEUROTROPHIC FACTOR;
D O I
10.1016/j.expneurol.2019.112977
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The incidence of depression is almost twice as high in the spinally injured population compared to the general population. While this incidence has long been attributed to the psychological, economic, and social burdens that accompany spinal cord injury (SCI), data from animal studies indicate that the biology of SCI may play an important role in the development of depression. Inflammation has been shown to impact stress response in rodents and humans, and inflammatory cytokines have been associated with depression for decades. The inflammation inherent to SCI may disrupt necessary mechanisms of mental homeostasis, such as serotonin production, dopamine production, and the hypothalamic pituitary adrenal axis. Additionally, gut dysbiosis that occurs after SCI can exacerbate inflammation and may cause further mood and behavior changes. These mediators combined may significantly contribute to the rise in depression seen after SCI. Currently, there are no therapies specific to depression after SCI. Elucidation of the molecular pathways that contribute to SCI-specific depression is crucial for the understanding of this disease and its potential treatments.
引用
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页数:13
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