Neuroinflammation and depression: A review.
Level 5 - mechanism / opinion, no new human data
Narrative review of preclinical and clinical mechanistic literature
PubMed 32150310 · doi:10.1111/ejn.14720
What was done
The authors reviewed preclinical and clinical evidence examining the role of neuroinflammation in major depressive disorder. The narrative review synthesized mechanisms linking brain immunity to three neurobiological correlates of depression: brain serotonin depletion, hypothalamic-pituitary-adrenal (HPA) axis dysregulation, and altered adult hippocampal neurogenesis in the dentate gyrus.
What was found
The abstract reports no numerical data or effect sizes. It describes mechanistic pathways: kynurenine pathway alteration toward excitotoxic components and HPA axis dysregulation converge to increase extracellular glutamate levels and transmission, reducing hippocampal neurogenesis. This cascade can be triggered or sustained by circulating peripheral inflammatory markers crossing the blood-brain barrier to activate microglia, primary central neuroinflammation (such as in neurodegenerative disorders), or chronic stress-induced vascular dysfunction driving microglial activation.
Why it matters
The review outlines how immune activation links monoaminergic, endocrine, and neurogenic pathways in depression, highlighting neuroinflammation as a potential therapeutic target.
Limits
This is a narrative review with no systematic search methodology, meta-analysis, or primary human data reported. The abstract provides qualitative mechanistic descriptions without quantitative estimates or risk-of-bias assessments.
Cited by
- context Under the influence of neuroinflammation, glutamate levels can spike up to one hundred times baseline, causing excitotoxicity that damages the blood-brain barrier, hippocampus, and mitochondrial membranes.