2011
DOI: 10.1371/journal.pone.0028668
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Cannabidiol Reduces Aβ-Induced Neuroinflammation and Promotes Hippocampal Neurogenesis through PPARγ Involvement

Abstract: Peroxisome proliferator-activated receptor-γ (PPARγ) has been reported to be involved in the etiology of pathological features of Alzheimer's disease (AD). Cannabidiol (CBD), a Cannabis derivative devoid of psychomimetic effects, has attracted much attention because of its promising neuroprotective properties in rat AD models, even though the mechanism responsible for such actions remains unknown. This study was aimed at exploring whether CBD effects could be subordinate to its activity at PPARγ, which has bee… Show more

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Cited by 363 publications
(342 citation statements)
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“…Here, the protective effects of CBD in an Aβ-induced neuroinflammatory mouse model were abolished by a PPARγ antagonist, but no evidence was given as to whether this was a direct or indirect effect [198]. CBD can also positively modulate COX via increased mRNA and protein expression of PPARγ and COX2, which also suggests that a COX2-generated increase in PGD 2 and 15d-PGJ 2 could underlie PPARγ activation in addition to any direct activation of PPARγ by CBD [18,54,93].…”
Section: Cbd Receptor Targets In Neurodegenerationmentioning
confidence: 90%
“…Here, the protective effects of CBD in an Aβ-induced neuroinflammatory mouse model were abolished by a PPARγ antagonist, but no evidence was given as to whether this was a direct or indirect effect [198]. CBD can also positively modulate COX via increased mRNA and protein expression of PPARγ and COX2, which also suggests that a COX2-generated increase in PGD 2 and 15d-PGJ 2 could underlie PPARγ activation in addition to any direct activation of PPARγ by CBD [18,54,93].…”
Section: Cbd Receptor Targets In Neurodegenerationmentioning
confidence: 90%
“…It should be noted that CBD is not particularly active at classic CB1 and CB2 receptors and, while it appears to be able to inhibit the inactivation of endocannabinoids (Bisogno et al, 2001), its mechanisms of action are quite diverse and extend to targets beyond the cannabinoid system (see Fernández-Ruiz et al, 2013). One of these targets includes the nuclear receptors of the PPAR family, in particular PPARγ (O'Sullivan and Kendall, 2010;Esposito et al, 2011). Here, we found that the inhibition of PPARγ completely blocked the motor benefits of CDB-BDS, clearly indicating the participation of these nuclear receptors in the effects of CBD-BDS on TMEV-IDD and presumably when it is combined with Δ 9 -THC-BDS in Sativex.…”
Section: Discussionmentioning
confidence: 99%
“…Thus, to determine how the CB1 and CB2 receptors influenced the effects of Δ 9 -THC-BDS, this phytocannabinoid was co-administered with a selective antagonist for the CB1 (AM251) or CB2 (AM630) receptor. In addition, as CBD appears to act through PPARγ (Esposito et al, 2011), and only negligibly through the CB1 and CB2 receptors (Izzo et al, 2009;Mecha et al, 2013b), CBD-BDS was also administered along with the PPARγ antagonist, T0070907. Our data indicated that the positive effect of Δ 9 -THC-BDS on motor deterioration was significantly blocked by the CB1 receptor antagonist AM251 and only partially by the CB2 receptor antagonist AM630 (Figure 2A).…”
Section: Figurementioning
confidence: 99%
“…O'Sullivan et al 35 O'Sullivan et al 35 O'Sullivan et al, 35 Esposito et al, 36 and De Filippis et al 37 …”
Section: Cbdmentioning
confidence: 99%
“…36 THC similarly has neuroprotective effects in a cell culture model of Parkinson's disease that was not inhibited by CB 1 , but was inhibited by a PPARγ antagonist. 34 In a model of multiple sclerosis, increasing local levels of endocannabinoids by inhibiting their uptake using UCM707, had neuroprotective effects against excitotoxicity which could be inhibited by CB 1 , CB 2 , and PPARγ antagonism.…”
mentioning
confidence: 96%