Abstract
lacking the neuronal cannabinoid CB1 receptor show a striking acceleration of the age-related cognitive decline, accompanied by an enhanced neuronal loss and increased neuroinflammation. A similar phenotype was also observed in mice lacking CB1 specifically on GABAergic neurons. The role of endogenous cannabinoids in age-related changes will also be addressed using knockout mouse models with deletions in endocannabinoid synthesizing and degrading enzymes.
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