Cannabidiol for Alzheimer's Disease Prevention (NCT05822362)
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clinical654 wordssynced 2026-04-02
Overview
flowchart TD
Cannabidiol_for_Alzheimer_s_Di["Cannabidiol for Alzheimers Disease Prevention NC"] -->|"references"| APOE["APOE"]
Cannabidiol_for_Alzheimer_s_Di["Cannabidiol for Alzheimers Disease Prevention NC"] -->|"references"| BDNF["BDNF"]
Cannabidiol_for_Alzheimer_s_Di["Cannabidiol for Alzheimers Disease Prevention NC"] -->|"references"| NLRP3["NLRP3"]
style Cannabidiol_for_Alzheimer_s_Di fill:#4fc3f7,stroke:#333,color:#000
This Phase 2 clinical trial investigates whether cannabidiol (CBD) can prevent or delay the onset of [Alzheimer's Disease](/diseases/alzheimers-disease) in individuals at elevated genetic risk for AD. The trial is conducted by researchers at the University of Colorado and represents a novel preventive therapeutic approach targeting the endocannabinoid system in at-risk populations.
Trial Details
| Parameter | Value | |-----------|-------| | NCT Number | NCT05822362 | | Phase | Phase 2 | | Enrollment | 236 participants | | Sponsor | University of Colorado | | Intervention | Cannabidiol (CBD) | | Purpose | Prevention | | Study Type | Interventional | | Allocation | Randomized, controlled |
Study Population
Target Population
Individuals at genetic risk for Alzheimer's Disease
May include carriers of Apolipoprotein E (APOE) ε4 allele or other known AD risk genetic variants
Cognitively normal at baseline
Rationale for Prevention in At-Risk Individuals
The rationale for CBD-based prevention in at-risk populations includes:
...
Overview
Mermaid diagram (expand to render)
This Phase 2 clinical trial investigates whether cannabidiol (CBD) can prevent or delay the onset of [Alzheimer's Disease](/diseases/alzheimers-disease) in individuals at elevated genetic risk for AD. The trial is conducted by researchers at the University of Colorado and represents a novel preventive therapeutic approach targeting the endocannabinoid system in at-risk populations.
Trial Details
| Parameter | Value | |-----------|-------| | NCT Number | NCT05822362 | | Phase | Phase 2 | | Enrollment | 236 participants | | Sponsor | University of Colorado | | Intervention | Cannabidiol (CBD) | | Purpose | Prevention | | Study Type | Interventional | | Allocation | Randomized, controlled |
Study Population
Target Population
Individuals at genetic risk for Alzheimer's Disease
May include carriers of Apolipoprotein E (APOE) ε4 allele or other known AD risk genetic variants
Cognitively normal at baseline
Rationale for Prevention in At-Risk Individuals
The rationale for CBD-based prevention in at-risk populations includes:
Genetic predisposition — APOE ε4 carriers and other genetic risk factors increase AD susceptibility by 3-12x
Neuroprotective mechanisms — CBD exerts multiple neuroprotective effects through the [endocannabinoid system](/mechanisms/endocannabinoid-system)
Early intervention opportunity — Preventive approaches before clinical symptoms may be more effective than symptomatic treatment
Safety profile — CBD has demonstrated an acceptable safety profile in previous clinical trials
Mechanism of Action
Cannabidiol (CBD) Neuroprotective Mechanisms
[CBD](/mechanisms/endocannabinoid-system) is a non-psychoactive phytocannabinoid that exerts neuroprotective effects through multiple pathways:
Anti-inflammatory effects
CB2 receptor activation on [microglia](/cell-types/microglia) shifts polarization from pro-inflammatory (M1) to anti-inflammatory (M2) phenotype
Suppression of [NLRP3 inflammasome](/mechanisms/nlrp3-inflammasome) assembly
Reduction in pro-inflammatory cytokines (TNF-α, IL-1β, IL-6)
Antioxidant properties
Direct scavenging of reactive oxygen species (ROS) through phenolic ring structure
Activation of Nrf2-dependent antioxidant gene expression
Protection against lipid peroxidation
Anti-excitotoxic effects
Modulation of glutamate release
Protection against NMDA receptor-mediated excitotoxicity
Calcium homeostasis maintenance
Neurotrophic support
Enhancement of [BDNF](/mechanisms/neurotrophic-factors) expression
Support of synaptic plasticity
Promotion of neurogenesis
Amyloid and tau modulation
Reduction of Aβ production through APP processing modulation