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

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.

Authors+Show Affiliations

Experimental and Clinical Neurosciences Laboratory, INSERM U1084, University of Poitiers, Poitiers, France. Laboratoire de Mathématiques et Applications (LMA), UMR CNRS 7348, Université de Poitiers, Poitiers, France.Centre de Recherche Clinique, Hôpital de Meaux, Meaux, France.Université de Poitiers et CHU de Poitiers, DACTIM, Laboratoire de Mathématiques et Applications, UMR CNRS 7348, SP2MI, Futuroscope, France.Laboratoire de Mathématiques et Applications (LMA), UMR CNRS 7348, Université de Poitiers, Poitiers, France. CHU Amiens Picardie, Université Picardie Jules Verne (UPJV), Amiens, France.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

28981597

Citation

Vallée, Alexandre, et al. "Effects of Cannabidiol Interactions With Wnt/β-catenin Pathway and PPARγ On Oxidative Stress and Neuroinflammation in Alzheimer's Disease." Acta Biochimica Et Biophysica Sinica, vol. 49, no. 10, 2017, pp. 853-866.
Vallée A, Lecarpentier Y, Guillevin R, et al. Effects of cannabidiol interactions with Wnt/β-catenin pathway and PPARγ on oxidative stress and neuroinflammation in Alzheimer's disease. Acta Biochim Biophys Sin (Shanghai). 2017;49(10):853-866.
Vallée, A., Lecarpentier, Y., Guillevin, R., & Vallée, J. N. (2017). Effects of cannabidiol interactions with Wnt/β-catenin pathway and PPARγ on oxidative stress and neuroinflammation in Alzheimer's disease. Acta Biochimica Et Biophysica Sinica, 49(10), pp. 853-866. doi:10.1093/abbs/gmx073.
Vallée A, et al. Effects of Cannabidiol Interactions With Wnt/β-catenin Pathway and PPARγ On Oxidative Stress and Neuroinflammation in Alzheimer's Disease. Acta Biochim Biophys Sin (Shanghai). 2017 Oct 1;49(10):853-866. PubMed PMID: 28981597.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of cannabidiol interactions with Wnt/β-catenin pathway and PPARγ on oxidative stress and neuroinflammation in Alzheimer's disease. AU - Vallée,Alexandre, AU - Lecarpentier,Yves, AU - Guillevin,Rémy, AU - Vallée,Jean-Noël, PY - 2017/02/14/received PY - 2017/06/23/accepted PY - 2017/10/6/entrez PY - 2017/10/6/pubmed PY - 2018/6/13/medline KW - Alzheimer's disease KW - GSK-3β KW - PI3K/Akt pathway KW - PPARγ KW - Wnt/β-catenin pathway KW - cannabidiol KW - neuroinflammation KW - oxidative stress SP - 853 EP - 866 JF - Acta biochimica et biophysica Sinica JO - Acta Biochim. Biophys. Sin. (Shanghai) VL - 49 IS - 10 N2 - 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. SN - 1745-7270 UR - https://www.unboundmedicine.com/medline/citation/28981597/Effects_of_cannabidiol_interactions_with_Wnt/β_catenin_pathway_and_PPARγ_on_oxidative_stress_and_neuroinflammation_in_Alzheimer's_disease_ L2 - https://academic.oup.com/abbs/article-lookup/doi/10.1093/abbs/gmx073 DB - PRIME DP - Unbound Medicine ER -