Researchers at the University of California, San Francisco, measured five different signaling molecules involved in inflammation in participants both before and after psilocybin treatment. The participants had significantly lower levels of inflammation following the treatments compared to baseline, and those changes persisted a month after the final dose. The team also tracked a blood marker of mitochondrial stress, finding substantial improvements immediately after psilocybin was given, though not during longer-term follow-up.
“This gives us an initial biological signal to investigate,” said Dr. Ellen Bradley, an associate professor of psychiatry at UCSF who helped lead the analysis.
The data come from a pilot study evaluating the feasibility and safety of giving psilocybin to people with Parkinson’s disease, a group typically excluded from psychedelic trials for safety concerns. The original study, published last year, found a “really promising safety profile” and that “symptoms even seemed to get a bit better,” Bradley said.
The researchers acknowledged limitations, including the lack of a control group and the fact that participants knew they were receiving the drug. The blood data need to be confirmed in follow-up studies before making definitive claims, said Aoife O’Donovan, a professor of psychiatry and behavioral sciences at UCSF and co-author of the paper. Still, O’Donovan said the findings reflect “objective markers” that changed over time, giving the team confidence to pursue this line of research.
Parkinson’s disease is characterized by dysregulated inflammation and mitochondrial dysfunction. The results raise the possibility that psychedelics could help address other diseases involving inflammation, said D. Parker Kelley, a research scientist at Columbia University and first author on the paper. “It’s a potential jumping off point for a lot more research in this area,” he said.
Charles Nichols, a professor at LSU Health Sciences Center who was not involved in the study but whose lab discovered anti-inflammatory effects of psychedelics about fifteen years ago, called the research “really exciting.” His lab’s early work found that a psychedelic acting on the 5-HT2A receptor functioned as a “potent anti-inflammatory,” even at doses well below those causing a psychoactive trip. He said the new study in Parkinson’s patients is a proof of principle, though “we can only draw so much from those conclusions.”