ReviewMolecular biology reports2026
Cannabidiol in Alzheimer's disease: evidence-weighted molecular mechanisms and translational challenges.
Review in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Alzheimer's disease (AD) is a complex, progressive neurodegenerative disorder in which amyloid-β accumulation, tau dysregulation, neuroinflammation, oxidative stress, mitochondrial dysfunction, synaptic loss and neurodegeneration interact to drive memory loss and cognitive decline. Despite advances in symptomatic therapies and anti-amyloid agents, clinical benefit remains modest, supporting interest in polypharmacological approaches. Cannabidiol (CBD) is a non-psychotropic phytocannabinoid that interacts with several signalling systems relevant to AD, including cannabinoid-related pathways, peroxisome proliferator-activated receptor-γ (PPARγ), transient receptor potential vanilloid 1 (TRPV1) channels, 5-HT1A signalling, fatty acid-binding proteins involved in anandamide transport, GPR55 and adenosine transporters. The most consistent preclinical findings indicate that CBD attenuates neuroinflammatory and oxidative responses and improves selected behavioural outcomes. Evidence for amyloid-related effects is supportive but heterogeneous. Direct evidence for tau modulation has expanded in transgenic and chemically induced models, but findings remain model-dependent, whereas mitochondrial rescue and adult hippocampal neurogenesis are less firmly established. Methodological variability in CBD source, formulation, dose, route, treatment window, sex, age and outcome selection limits direct comparison between studies. Work on other cannabinoids and CBD:Δ9-THC combinations is discussed for context, and current evidence does not establish CBD as a disease-modifying treatment in AD. Overall, current preclinical evidence supports continued investigation of CBD as a multi-target neuroprotective candidate in AD, provided that future studies use standardized, mechanism-focused and translationally relevant designs. This review compares preclinical evidence across pathological domains and identifies translational research priorities.
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Identifiers
42909680What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.