Hypothetical model of how modulation of CB
receptors may attenuate inflammation in AD. 1. Activated astrocytes, microglia, and macrophages release proinflammatory cytokines such as IL-1β, IL-6, and TNF-alpha in response to the deposition and accumulation of Aβ and the release of chemoattractants from damaged neurons. The endocannabinoid system counter regulates such processes and CB2 receptors seem fundamentally involved in this response. 2. MH modulates CB2 receptors, leading to inhibition of TH1 cytokines and possibly decreased chemotaxis 3. Decreased inflammation promotes Aβ phagocytosis (clearance) and neuronal viability.