Psychedelics in neuroinflammation: Mechanisms and therapeutic potential.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms and pathways without systematic review or original human empirical data.
PubMed 39892847 · doi:10.1016/j.pnpbp.2025.111278
What was done
This narrative review summarizes the proposed molecular mechanisms and therapeutic potential of psychedelics, including psilocybin, lysergic acid diethylamide (LSD), and dimethyltryptamine (DMT), in targeting neuroinflammation associated with conditions such as Alzheimer's disease, Parkinson's disease, and major depressive disorder.
What was found
The abstract reports purely qualitative mechanistic descriptions and does not provide quantitative findings or numerical effect sizes. It details that psychedelics act primarily through serotonin 5-HT2A receptors to regulate microglial activity, alter pro-inflammatory cytokine production, modulate neuroprotective versus neurotoxic metabolites, and activate NF-κB, PI3K/Akt, and mTOR signaling pathways, with additional contributions from glutamatergic, dopaminergic, noradrenergic, GABAergic, and cholinergic neurotransmission.
Why it matters
It outlines the biological rationale for using serotonergic psychedelics to counteract neuroinflammatory pathways in neurodegenerative and psychiatric disorders.
Limits
The abstract describes a non-systematic narrative review with no quantitative data, sample sizes, or study selection criteria provided. The described biological mechanisms rely heavily on preclinical models and theoretical pathways that require validation in controlled clinical trials before therapeutic efficacy in humans can be confirmed.
Cited by
- contradicts All euphoric substances are neurotoxic.