An analysis of 12 people with Parkinson’s disease found lower blood inflammation markers after psilocybin sessions, offering a biological lead for research while leaving treatment effects and clinical value unresolved.
JAMA Psychiatry published the analysis online Oct. 21. It examines inflammation and mitochondrial stress markers in people with Parkinson’s disease and mood dysfunction. The journal classifies the work as nonrandomized and single-arm; it uses data from an earlier pilot rather than a controlled comparison.
In that pilot, participants received 10 milligrams of psilocybin, then 25 milligrams about two weeks later, alongside psychotherapy. The pilot was designed to assess feasibility and safety.
NPR reported that researchers found lower levels of five inflammation-related signaling molecules in blood after the two sessions. The outlet said the lower readings were still present at a follow-up one month after the final dose. NPR also reported a short-term improvement in a blood marker of mitochondrial stress, but said that change was absent at a later assessment.
The study did not include a comparison group, and participants knew they were receiving psilocybin, NPR reported. Without those safeguards, the observed changes cannot establish that the drug caused them. The biomarker analysis also does not show that treatment improved patients’ symptoms.
The paper identifies inflammation and mitochondrial stress as features of Parkinson’s disease that could play a role in mood and motor symptoms. Ellen R. Bradley, an associate professor of psychiatry at the University of California, San Francisco, told NPR: “This gives us an initial biological signal to investigate.”
The University of California, San Francisco, has described a larger randomized study with Yale University as a next step. UCSF’s summary sets a 100-person target for the larger study. Its trial registry lists expected enrollment of 60 and estimates completion around June 2028.
