Brain Inflammation

Neuroinflammation is addressable through food choices alone, without pharmacological intervention. Mechanical concussion-related inflammation and environment-driven neuroinflammation can involve similar brain inflammatory processes but arise from different causes. Advanced TRD interventions produce downstream healthcare costs 4.3 times higher than standard care. TNF-alpha blockers have been explored experimentally for depression because depression involves TNF-alpha-mediated inflammation, validating the inflammatory mechanism. Chronic stress dysregulates the HPA axis, leading to increased blood-brain barrier permeability. Once peripheral inflammatory markers enter the CNS, microglia activate and produce quinolinic acid and other neurotoxic mediators damaging mood and cognition circuits. Neuroinflammation is presented as a likely driver of many concussion-related symptoms and syndromes. Borrelia and co-infections can disrupt the blood-brain barrier through systemic inflammatory signaling. Serotonin, dopamine, and norepinephrine deficits in depression are downstream outputs of inflammatory dysregulation, not primary deficits. Microglial activation is presented as a hallmark of Lyme-…