Cannabidiol reduces Abeta-induced neuroinflammation and promotes hippocampal neurogenesis through PPARgamma 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 been recently indicated as its putative binding site. CBD actions on β-amyloid-induced neurotoxicity in rat AD models, either in presence or absence of PPAR antagonists were investigated. Results showed that the blockade of PPARγ was able to significantly blunt CBD effects on reactive gliosis and subsequently on neuronal damage. Moreover, due to its interaction at PPARγ, CBD was observed to stimulate hippocampal neurogenesis. All these findings report the inescapable role of this receptor in mediating CBD actions, here reported.


Autore Pugliese

Tutti gli autori

  • CARRATU' M.R.

Titolo volume/Rivista

Non Disponibile


Anno di pubblicazione

2011

ISSN

1932-6203

ISBN

Non Disponibile


Numero di citazioni Wos

92

Ultimo Aggiornamento Citazioni

Non Disponibile


Numero di citazioni Scopus

103

Ultimo Aggiornamento Citazioni

Non Disponibile


Settori ERC

Non Disponibile

Codici ASJC

Non Disponibile