A recent study published in BMC Neuroscience highlights psilocybin’s potential neuroprotective effects.
Conducted by researchers from Taiwan National Health Research Institutes, China Medical University, and University Hospitals of Cleveland, the study explored how psilocybin—a 5HT2A receptor agonist found in “magic mushrooms”—can reduce brain damage and enhance neurological recovery after stroke.
The study involved adult male and pregnant Sprague-Dawley rats, which were subjected simulated stroke conditions. Psilocybin was administered either before or shortly after the induced stroke.
Results showed that pretreatment with psilocybin significantly reduced brain infarction and improved locomotor function in the rats. Additionally, psilocybin reduced glutamate-mediated neuronal loss in cortical cultures, effects that were reversed when the BDNF inhibitor ANA12 was used, suggesting psilocybin’s protective mechanisms are linked to brain-derived neurotrophic factor (BDNF) signaling.
Furthermore, rats treated with psilocybin after the stroke exhibited better recovery in locomotor behavior and upregulation of key neural proteins such as MAP2 and synaptophysin, while inflammatory markers like IBA1 were downregulated.
“Psilocybin reduced brain infarction and improved locomotor behavior in stroke rats; the protective mechanisms involve regulating BDNF expression. Our data support a novel therapeutic approach of psilocybin in stroke”, claim researchers.
Below is the study’s full abstract. The study’s full text can be found here.
Abstract
Background: Psilocybin is a psychedelic 5HT2A receptor agonist found in “magic mushrooms”. Recent studies have indicated that 5HT2A agonists, such as dimethyltryptamine, given before middle cerebral artery occlusion (MCAo), improve staircase behavior, increased BDNF expression, and reduce brain infarction in stroke rats. The objective of this study is to determine the protective effect of psilocybin in cellular and animal models of stroke.
Methods: Adult male and timed-pregnant Sprague-Dawley rats were used for this study. The neural protective effects of psilocybin were determined in primary rat cortical neurons and adult rats. Rats were subjected to a 60-min middle cerebral artery occlusion. Brain tissues were collected for histological and qRTPCR analysis.
Results: Psilocybin reduced glutamate-mediated neuronal loss in rat primary cortical neuronal cultures. Psilocybin-mediated protection in culture was antagonized by the BDNF inhibitor ANA12. Pretreatment with psilocybin reduced brain infarction and neurological deficits in stroke rats. Early post-treatment with psilocybin improved locomotor behavior, upregulated the expression of MAP2 and synaptophysin, and down-regulated the expression of IBA1 in the stroke brain. ANA12 significantly attenuated psilocybin-mediated reduction in brain infarction and improvements in locomotor behavior.
Conclusions: Psilocybin reduced brain infarction and improved locomotor behavior in stroke rats; the protective mechanisms involve regulating BDNF expression. Our data support a novel therapeutic approach of psilocybin in stroke.
