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.