TABLE 2.

CBD on AD, in vitro study.

Cell used	Major effects on CBD treatment	Ref.
PC12 cells	Protects PC12 neuronal cells from Aβ peptide (1 ug/mL)-induced neurotoxicity upon pre-exposure via inhibition of lipid peroxidation and downregulation of caspase 3	Iuvone et al. (2004)
PC12 cells	Inhibits Aβ-induced hyperphosphorylation of tau protein via reduction of the phosphorylation of GSK-3β	Esposito et al. (2006)
PC12 cells	Inhibits production of NO and iNOS protein via the downregulation of NF-κB and phosphorylated p38 MAPK	Esposito et al. (2006)
Culture astrocytes and primary rat astrocytes	PPARγ-mediated inhibition of reactive gliosis (suppresses GPAF expression) and neuroinflammation	Esposito et al. (2011)
Bv-2 microglia cells	Inhibition of LPS-induced microglial activation by the downregulation of NF-κB and IFN (beta)-STAT pathways	Kozela et al. (2010)
Neuronal SHSY5YAPP+ cells	Promotes ubiquitination of APP and lowers the expression of Aβ peptide by activating PPARγ	Scuderi et al. (2014)
Cultured N13 microglial cells and primary microglia cells (BV-2)	Reduces microglial activation via CB2 and A2A receptor-mediated inhibition of ATP-induced increase in intracellular Ca2+ and thereby microglial cell migration in addition to the anti-inflammatory effect of CBD.	Martín-Moreno et al. (2011)
Human mesenchymal stem cells (hMSCs)	Pretreatment downregulates kinase responsible for tau phosphorylation, specifically the PI3K/Akt/GSK-3β pathway and secretase genes responsible for Aβ production. Effect is mediated via TRVP1 receptor	Libro et al. (2016)
Mesenchymal stem cells	Migration of MSc is mediated via the CB2 receptor and the GPR55 receptor by activation of the p42/44 MAPK pathway	Schmuhl et al. (2014)
Hippocampal slice of C57 mice perfused with Aβ	Pretreatment recovers the synaptic transmission attenuated by Aβ	Hughes and Herron (2019)