Cited by 228Alzheimer's disease research and treatmentsCannabis and Cannabinoid ResearchMedicinal Plants and Neuroprotection

Effects of cannabidiol interactions with Wnt/β-catenin pathway and PPARγ on oxidative stress and neuroinflammation in Alzheimer's disease

Vallée, Alexandre, Lecarpentier, Yves, Guillevin, Rémy, Vallée, Jean-Noël·2017·Acta Biochimica et Biophysica Sinica

Abstract

Alzheimer's disease (AD) is a neurodegenerative disease, in which the primary etiology remains unknown. AD presents amyloid beta (Aβ) protein aggregation and neurofibrillary plaque deposits. AD shows oxidative stress and chronic inflammation. In AD, canonical Wingless-Int (Wnt)/β-catenin pathway is downregulated, whereas peroxisome proliferator-activated receptor γ (PPARγ) is increased. Downregulation of Wnt/β-catenin, through activation of glycogen synthase kinase-3β (GSK-3β) by Aβ, and inactivation of phosphatidylinositol 3-kinase/Akt signaling involve oxidative stress in AD. Cannabidiol (CBD) is a non-psychotomimetic phytocannabinoid from Cannabis sativa plant. In PC12 cells, Aβ-induced tau protein hyperphosphorylation is inhibited by CBD. This inhibition is associated with a downregulation of p-GSK-3β, an inhibitor of Wnt pathway. CBD may also increase Wnt/β-catenin by stimulation of PPARγ, inhibition of Aβ and ubiquitination of amyloid precursor protein. CBD attenuates oxidative stress and diminishes mitochondrial dysfunction and reactive oxygen species generation. CBD suppresses, through activation of PPARγ, pro-inflammatory signaling and may be a potential new candidate for AD therapy.

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Crossref · 10.1093/abbs/gmx073

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243 of 243 references verified0 citation errors · 0 not checkable

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  • In PC12 neuronal cells, CBD has shown inhibition of tau hyperphosphorylation.

    “In PC12 neuronal cells, CBD has shown protection against oxidative stress, Aβ-induced neurotoxicity, inhibition of tau hyperphosphorylation, prevention of proinflammatory gene transcription, and inhibition of Aβ-induced tau hyperphosphorylation [188,189].”
  • In PC12 neuronal cells, CBD has shown protection against oxidative stress and Aβ-induced neurotoxicity.

    “In PC12 neuronal cells, CBD has shown protection against oxidative stress, Aβ-induced neurotoxicity, inhibition of tau hyperphosphorylation, prevention of proinflammatory gene transcription, and inhibition of Aβ-induced tau hyperphosphorylation [188,189].”
  • In PC12 neuronal cells, CBD has shown prevention of proinflammatory gene transcription.

    “In PC12 neuronal cells, CBD has shown protection against oxidative stress, Aβ-induced neurotoxicity, inhibition of tau hyperphosphorylation, prevention of proinflammatory gene transcription, and inhibition of Aβ-induced tau hyperphosphorylation [188,189].”

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Authors
Vallée, A., Lecarpentier, Y., Guillevin, R., & Vallée, J.-N.
Affiliations
Centre National de la Recherche Scientifique (FR)
Venue
Acta Biochimica et Biophysica Sinica
Published
2017-10-01
Volume
49
Issue
10
Pages
853-866
ISSN
1672-9145 (ISSN-L)
OpenAlex
W2738129635
Cited by
226
References
244
Citations by year
2026: 20 · 2025: 17 · 2024: 26 · 2023: 29 · 2022: 37 · 2021: 37 · 2020: 31 · 2019: 16 · 2018: 9 · 2017: 4
FWCI
12.18
Type
journal article
Language
en
Open access
closed
Locations
  • Acta Biochimica et Biophysica Sinica (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
  • Health Sciences › Medicine › Complementary and alternative medicine › Medicinal Plants and Neuroprotection
Keywords
cannabidiol, Alzheimer's disease, Wnt/β-catenin signaling, PPARγ, oxidative stress, neuroinflammation, amyloid-beta, glycogen synthase kinase-3β, tau hyperphosphorylation, phosphatidylinositol 3-kinase/Akt signaling, mitochondrial dysfunction, reactive oxygen species, neuroprotection
MeSH terms
Glycogen Synthase Kinase 3 beta, Alzheimer Disease, Animals, Cannabidiol, Inflammation, Models, Biological, Phosphorylation, Amyloid beta-Peptides, PC12 Cells, Neurofibrillary Tangles, tau Proteins, Oxidative Stress, PPAR gamma, Rats, Wnt Signaling Pathway

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