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Leelavathi N Madhu1, Yogish Somayaji2, Sanya Kotian1

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Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 25, 2025
PubMed
Summary
This summary is machine-generated.

Psilocybin treatment improved cognitive function and reduced neuroinflammation in a mouse model of Alzheimer's disease (AD). This suggests psilocybin may offer a novel therapeutic avenue for AD by enhancing brain function and neurogenesis.

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Alzheimer's Disease Research

Background:

  • Chronic neuroinflammation is a key driver of Alzheimer's disease (AD) pathogenesis, leading to cognitive and mood decline.
  • Current Alzheimer's therapies are limited in their ability to halt disease progression.
  • Psilocybin, known for its efficacy in treating depression, demonstrates potential in reducing neuroinflammation and promoting hippocampal neurogenesis.

Purpose of the Study:

  • To investigate the efficacy of psilocybin in mitigating cognitive decline in a 5x familial Alzheimer's disease (5xFAD) mouse model.
  • To assess psilocybin's impact on neuroinflammation, neurogenesis, and synaptic function in the context of AD.

Main Methods:

  • Monthly administration of psilocybin (0.5mg/Kg) or vehicle to 5xFAD mice for 4 months.
  • Neurobehavioral testing to evaluate cognitive and mood functions post-treatment.
  • Analysis of brain tissues for neuroinflammation markers, hippocampal neurogenesis, synapse loss, and amyloid-beta plaques; hippocampal proteomics was also performed.

Main Results:

  • Psilocybin-treated mice showed enhanced cognitive functions, including pattern separation and associative recognition memory, and lacked anhedonia compared to vehicle-treated controls.
  • Significant reductions in neuroinflammatory markers (NLRP3 inflammasome, p38 MAPK, cGAS-STING signaling) were observed in psilocybin-treated mice.
  • Increased neurogenesis, improved BDNF-ERK-CREB signaling, and preserved synaptic proteins were noted, alongside proteomic evidence of upregulated proteins involved in neuroinflammation, mTOR signaling, and synaptic function.

Conclusions:

  • Psilocybin treatment effectively maintained cognitive function in an AD mouse model without altering amyloid-beta plaque load.
  • The observed cognitive benefits are attributed to psilocybin-induced reduction in neuroinflammation, enhanced hippocampal neurogenesis, and synaptic preservation.