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A small, open-label trial found that an inflammatory index was lower than baseline at follow-up after psilocybin therapy in people with Parkinson’s disease and mood dysfunction. Some mitochondrial stress marker changes were short-lived, and the researchers say larger randomized trials are needed to test whether the findings are consistent or related to clinical benefits.
A small, nonrandomized trial found that an index of systemic inflammation remained below baseline at follow-up after psilocybin therapy in people with Parkinson’s disease and mood dysfunction, according to a research letter by University of California, San Francisco researchers. The study included 12 participants, and the results are preliminary: they do not show that psilocybin treats Parkinson’s disease or that changes in blood markers cause clinical improvement.
Ellen Bradley, MD, and colleagues studied 12 people aged 40 to 75 with mild-to-moderate Parkinson’s disease. Participants received oral synthetic psilocybin at 10 mg and 25 mg, approximately two weeks apart. The open-label study had no control group, and plasma samples were available from nine participants for analysis.
The researchers measured inflammation at baseline, one day after each dose, and 30 days after the 25-mg dose. Their proinflammatory index combined measurements of IL-6, IL-8, tumor necrosis factor alpha, interferon gamma and high-sensitivity C-reactive protein. Compared with baseline, the index was lower one day after 10 mg (standard mean difference, or SMD, −0.72; adjusted P=0.003), one day after 25 mg (SMD −0.60; adjusted P=0.02), and 30 days after 25 mg (SMD −0.62; adjusted P=0.047).
Changes in individual markers were not uniform. IL-6 was significantly lower and IL-10 significantly higher one day after the 10-mg dose, but those changes were not significant at other measured times. The mitochondrial stress marker GDF-15 was lower one day after both doses, but not 30 days after the 25-mg dose. FGF-21 rose one day after each dose, though the increase was not statistically significant.
What the Blood Markers May Show
The results add preliminary biological data to research on psilocybin beyond psychiatric conditions. In this study, the inflammatory index was lower at each reported follow-up than at baseline, while the GDF-15 changes did not persist to the 30-day measurement. That contrast makes the timing and durability of any biological effects an important question for further research.
The findings do not establish that psilocybin reduces inflammation in Parkinson’s disease generally, slows disease progression, or improves symptoms through an anti-inflammatory effect. The trial was small, had no comparison group, and measured blood markers in only nine participants. It also cannot separate possible drug effects from other factors that may affect measurements over time. Larger controlled studies will be needed to test whether the changes can be replicated and whether they relate to health outcomes patients notice.
How This Fits Parkinson’s Research
The research letter’s authors said the biomarker analysis was connected to a parent trial of psilocybin therapy in Parkinson’s patients with mood dysfunction. The source report said that earlier trial found an association with reduced depression, anxiety and motor symptoms. Those reported clinical associations do not establish that changes in inflammation or mitochondrial stress explain any symptom changes.
Study co-author Aoife O’Donovan, PhD, told MedPage Today that the team is following up with more detailed analyses in a randomized controlled trial involving people with Parkinson’s disease. Albert Garcia-Romeu, PhD, of Johns Hopkins University School of Medicine, who was not involved, described the work as part of a broader effort to examine biological effects of psychedelics in non-psychiatric conditions. His comments provide outside perspective, not independent confirmation of the trial’s results.
“To our knowledge, this is the first report of changes in these types of markers after psychedelic treatment in people with a neurodegenerative disease.”
— Ellen Bradley, MD, University of California, San Francisco, speaking to MedPage Today
Limits of the Initial Findings
The study’s small sample, open-label design and lack of a control group limit what can be concluded. Biomarker analyses used samples from nine of the 12 participants, and the report does not establish whether the observed differences would appear in a larger or more diverse group. It is also unclear whether the marker changes are directly due to psilocybin, how long any effects might last beyond the measured period, or whether they are connected to depression, anxiety or motor symptoms.
The reported statistical differences are comparisons with participants’ own baseline measurements, not evidence that psilocybin outperformed a placebo or standard treatment. The results should not be taken as proof of a treatment for Parkinson’s disease.
Controlled Trial Will Test Replication
UCSF researchers are conducting a randomized controlled trial in Parkinson’s disease patients, with more in-depth analyses of inflammation and mitochondrial stress, O’Donovan told MedPage Today. Those results may help establish whether the initial biomarker patterns recur under a controlled design. The source report did not provide a completion date or results timeline for that Parkinson’s trial.
Until further results are available, the current findings remain preliminary. Researchers will need to clarify whether the marker changes are reproducible, how long they last, and whether they correspond to measurable clinical outcomes.
Key Questions
What did the Parkinson’s trial find?
The study reported that a combined inflammation index was lower than baseline one day after both psilocybin doses and 30 days after the 25-mg dose. It also found short-term changes in some individual markers.
How many people took part?
Twelve people with mild-to-moderate Parkinson’s disease and mood dysfunction enrolled. Plasma samples used for the biomarker analysis were available from nine participants.
Does this show psilocybin treats Parkinson’s disease?
No. The study was small, open-label and nonrandomized, and it measured blood markers. It does not establish that psilocybin treats Parkinson’s, slows its progression, or causes symptom improvements through changes in inflammation.
What happens next?
The UCSF researchers are following up with more detailed biomarker analyses in a randomized controlled trial involving people with Parkinson’s disease. The report did not give a date for those results.
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