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) via PubMed
Summary
AI-generated from the abstractAlzheimer's disease accounts for 60% of dementia cases, and no cure exists. Recent research suggests psychedelics may reduce neuroinflammation by activating 5HT2A receptors, lowering proinflammatory cytokines such as TNF-α and IL-6. Additionally, psychedelics may promote neuroplasticity by increasing brain-derived neurotrophic factor (BDNF) levels through sigma-1 receptor stimulation. This review examines these potential effects on Alzheimer's disease from neuroinflammatory and neuroplasticity perspectives.
Study at a glance
| Characteristics | Review Peer reviewed |
|---|---|
| Topics | Neuroplasticity |
| Keywords | 5-HT Receptors Alzheimer’s disease Neuroinflammation Psychedelics |
| Key finding | 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.