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Potential sites of action of the cannabinoid system for the treatment of AD. Activation of the CB2 receptor reduces the formation of reactive oxygen species (ROS) and the release of interleukin-1β from microglia, thus exerting an anti-inflammatory effect. In neurones, activation of the CB1 receptor reduces intracellular Ca2+ concentration ([Ca2+]i), protects against oxidative stress and reduces inflammatory signalling by inhibition of nuclear factor κB. CB1 activation also inhibits glutamate release to reduce excitotoxicity, and enhances neurotrophin expression and neurogenesis. CBD is neuroprotective and anti-inflammatory in a CB receptor-independent manner, and also reduces tau phosphorylation. Δ9-THC inhibits AChE, resulting in enhanced cholinergic transmission and reduced amyloidogenesis. AD, Alzheimer' disease; AChE, acetylcholinesterase; CB, cannabinoid; CBD, cannabinoid; Δ9-THC, Δ9-tetrahydrocannabinol.