SynthesisInternational journal of molecular sciences2025
Therapeutic Potential for Cannabidiol on Alzheimer's Disease-Related Neuroinflammation: A Systematic Review and Meta-Analysis.
Synthesis in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Lipidomic Evidence for Cannabidiol-Induced Remodeling of Cellular Lipid Composition in SH-SY5Y Cells.Cells · 2026Article
- Targeting Pain and Depression in Alzheimer's Disease: Translational Insights and Emerging Treatments.Pharmaceuticals (Basel, Switzerland) · 2026Review
Corrections and comments
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Authors and funding
3 authors.
Funding
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Abstract
Alzheimer's disease (AD) is a pervasive neurodegenerative disorder characterized by chronic neuroinflammation; current interventions primarily offer symptomatic relief. Cannabidiol (CBD), a non-psychoactive phytocannabinoid, exhibits multi-target therapeutic potential due to its established anti-inflammatory and neuroprotective properties. While growing interest exists, the evidence regarding CBD's effects on AD-related neuroinflammation has not been robustly consolidated in a quantitative meta-analysis. Therefore, this article reviews the current literature around CBD related to its potential in alleviating neuroinflammation, followed by a meta-analysis of preclinical and clinical studies using random-effects modeling to assess CBD efficacy on neuroinflammation and clinical outcomes in AD. In preclinical AD models, the meta-analysis demonstrated that CBD significantly and consistently reduced key markers of neuroinflammation and reactive gliosis, specifically glial fibrillary acidic protein (GFAP) (
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