Skip to content

The immunomodulatory effects of psychedelics in Alzheimer's disease-related dementia.

Alireza Mohammad Hosseini, Hossein Khaleghzadeh-Ahangar, Atena Rahimi

Neuroscience January 9, 2025 DOI: 10.1016/j.neuroscience.2024.11.062 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Review Peer reviewed
Topics Neuroplasticity
Keywords 5-HT Receptors Alzheimer’s disease Neuroinflammation Psychedelics Sigma-1 receptor
Key findings Psychedelics may reduce neuroinflammation and promote neuroplasticity in Alzheimer's disease through 5HT2A receptor activation and sigma-1 receptor stimulation.

Abstract

Dementia is an increasing disorder, and Alzheimer's disease (AD) is the cause of 60% of all dementia cases. Despite all efforts, there is no cure for stopping dementia progression. Recent studies reported potential effects of psychedelics on neuroinflammation during AD. Psychedelics by 5HT2AR activation can reduce proinflammatory cytokine levels (TNF-α, IL-6) and inhibit neuroinflammation. In addition to neuroinflammation suppression, psychedelics induce neuroplasticity by increasing Brain-derived neurotrophic factor (BDNF) levels through Sigma-1R stimulation. This review discussed the effects of psychedelics on AD from both neuroinflammatory and neuroplasticity standpoints.

Comparable studies

Other narrative reviews on neuroplasticity, most cited first.

Citations in the library

Explore topics