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In a small, open-label study of people with Parkinson’s disease and mood dysfunction, an index of systemic inflammation was lower at follow-up after two psilocybin doses. Some mitochondrial stress marker changes were short-lived, and the findings do not establish that psilocybin reduces inflammation or improves Parkinson’s symptoms. Researchers say randomized trials are needed.
A small, open-label trial in people with Parkinson’s disease and mood dysfunction found that a measured index of systemic inflammation was lower after participants received psilocybin, according to results reported October 21. The study involved 12 participants and had no control group, so it cannot establish that psilocybin caused the changes or that they led to clinical benefits.
Ellen Bradley, MD, of the University of California, San Francisco, and colleagues studied adults ages 40 to 75 with mild-to-moderate Parkinson’s disease. Participants received oral synthetic psilocybin at doses of 10 mg and 25 mg about two weeks apart. The researchers collected plasma samples from nine participants at baseline, one day after each dose, and 30 days after the 25-mg dose.
The primary inflammation measure combined levels of five markers: IL-6, IL-8, tumor necrosis factor alpha, interferon gamma and high-sensitivity C-reactive protein. Compared with baseline, the combined index was lower one day after the 10-mg dose (standard mean difference, or SMD, −0.72; adjusted P=0.003), one day after the 25-mg dose (SMD −0.60; adjusted P=0.02), and 30 days after the 25-mg dose (SMD −0.62; adjusted P=0.047).
Changes in individual markers did not all persist. IL-6 was significantly lower, and IL-10 higher, one day after the 10-mg dose, but neither difference was reported at later follow-ups. The mitochondrial stress marker GDF-15 was lower one day after each dose but not at the 30-day measurement. FGF-21 rose after each dose, though the increase was not statistically significant. The findings appeared in a research letter in JAMA Psychiatry.
Inflammation Signals Need Testing
The results offer an early biological observation in a population where research on psychedelic treatment has mostly focused on mood and other psychiatric conditions. The study adds measurements of inflammation and mitochondrial stress to an ongoing inquiry into how psilocybin might affect people with a neurological disorder.
That does not show that the marker changes explain symptom improvement. The source report says the parent trial had found an association between psilocybin therapy and reduced depression, anxiety and motor symptoms, but the current biomarker study was small and nonrandomized. It cannot determine whether the inflammation changes were caused by treatment, whether they matter to Parkinson’s disease, or whether they correspond to benefits patients can feel. The findings are best treated as a basis for further research, not evidence of an established treatment effect.
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How the Parkinson’s Study Worked
The research was an open-label study: participants and researchers knew psilocybin was being given, and the study did not include a comparison group receiving a placebo or another treatment. Although 12 people took part, blood samples for the reported analyses were available from nine participants. These features limit how confidently the results can be generalized or linked to psilocybin.
The report places the biomarker work alongside a parent trial that examined psilocybin therapy in Parkinson’s patients with mood dysfunction. It also reflects broader research interest in possible biological effects of psychedelics beyond mental health. Albert Garcia-Romeu, PhD, of Johns Hopkins University, who was not involved, told MedPage Today that much prior work on psilocybin and LSD had focused on conditions such as depression, anxiety and addiction. He described the Parkinson’s findings as evidence that warrants more study, not proof of a mechanism or clinical effect.
“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
What the Markers Cannot Show
The study does not establish that psilocybin caused the changes, because it was small and lacked randomization and a control group. Blood samples were analyzed for nine participants, and the report does not establish whether the marker patterns would appear in a larger or more diverse Parkinson’s population.
It also remains unclear whether the changes in inflammation or GDF-15 relate to Parkinson’s symptoms, disease progression, or meaningful outcomes for patients. The GDF-15 reduction was not present at the 30-day follow-up, while the reported FGF-21 increases were not statistically significant. The available findings do not show that psilocybin is an approved or established treatment for Parkinson’s disease.
Randomized Trial Will Test Findings
O’Donovan told MedPage Today that the researchers are following up with more detailed analyses of inflammation and mitochondrial stress in a randomized controlled trial involving Parkinson’s patients. That work can help test whether the initial changes recur under a stronger study design. The report does not give a completion date or results timeline for that trial.
Garcia-Romeu also said his group was studying psilocybin in people with mild cognitive impairment or early-stage Alzheimer’s disease and depression. At the time of the report, his team had treated 18 people and enrolled 19 of a planned 20, with publication expected the following year. Those results are separate from the Parkinson’s study and will not, by themselves, confirm its findings.
Key Questions
What did the Parkinson’s trial find?
The study reported a lower combined systemic inflammation index at several follow-up points after psilocybin. It also found a temporary reduction in the mitochondrial stress marker GDF-15.
How many people were included?
Twelve people with mild-to-moderate Parkinson’s disease and mood dysfunction took part. Plasma samples used for the biomarker analysis were collected from nine participants.
Does this show psilocybin treats Parkinson’s disease?
No. The study was small, open-label and nonrandomized, and it had no control group. Its results do not establish that psilocybin caused the marker changes or that those changes improve symptoms or disease outcomes.
What research is planned next?
The UCSF researchers said they are examining inflammation and mitochondrial stress in a randomized controlled trial involving Parkinson’s patients. Results and a completion timeline were not provided in the report.
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