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Publication

β-Amyloid exacerbates inflammation in astrocytes lacking fatty acid amide hydrolase through a mechanism involving PPAR-α, PPAR-γ and TRPV1, but not CB₁ or CB₂ receptors.

Cristina Benito | Rosa María Tolón | Ana Isabel Castillo | Lourdes Ruiz-Valdepeñas | José Antonio Martínez-Orgado | Francisco Javier Fernández-Sánchez | Carmen Vázquez | Benjamin F Cravatt | Julián Romero
British journal of pharmacology | 2012

The endocannabinoid system may regulate glial cell functions and their responses to pathological stimuli, specifically, Alzheimer's disease. One experimental approach is the enhancement of endocannabinoid tone by blocking the activity of degradative enzymes, such as fatty acid amide hydrolase (FAAH).

Pubmed ID: 22321194

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