Depression following a traumatic brain injury: uncovering cytokine dysregulation as a pathogenic mechanism

Traumatic brain injury (TBI) can lead to long-term complications, including depression, which can affect various aspects of life such as work and cognitive function. The exact cause of depression after TBI is unclear, but inflammation in the brain may play a role. TBI can cause ongoing inflammation in the brain, and this inflammation might contribute to depression. Cytokines, which are inflammatory molecules, are elevated after TBI and can affect how brain cells communicate. This review discusses the evidence supporting the idea that inflammation is linked to depression after TBI, focusing on how specific inflammatory molecules like TNFα and IL-1 could disrupt brain function and lead to depression.

• 1
  TBI-induced inflammation, characterized by elevated cytokines, is a potential mechanism for post-TBI depression.
• 2
  Cytokines such as TNFα and IL-1 can directly alter neuronal synaptic physiology, potentially contributing to depression.
• 3
  Targeting inflammation through neuroimmune modulation may be a promising area of treatment for the psychological complications of TBI.