SCI and depression: Does inflammation commandeer the brain?
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Updated: Jan 23, 2026

Stab-Wound Mouse Model for Studying Hemorrhage and Inflammation in Traumatic Brain Injury
Published on: February 21, 2025
Kiralyn Brakel1, Michelle A Hook1
1School of Medicine, Department of Neuroscience and Experimental Therapeutics, Texas A&M University, Medical Research and Education Building, Ste. 1005, 8447 Riverside Pkwy, Bryan, TX 77807, United States; Texas A&M Institute of Neuroscience, Texas A&M University, Interdisciplinary Life Sciences Building, Rm 3148, 3474 College Station, TAMU, TX, United States.
Abstract:
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.
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