Inhibition of microglial activation and polarization

The "inhibition of microglial activation and polarization" refers to strategies for reducing the pro-inflammatory (often "M1") activation state of microglia in the central nervous system, thereby decreasing the release of neurotoxic mediators such as cytokines, nitric oxide, and reactive oxygen species. Many neurodegenerative and neuroinflammatory disorders are associated with chronic microglial activation, contributing to neuronal damage and disease progression. Inhibiting this activation, or promoting a shift to an anti-inflammatory ("M2") phenotype, is being explored with drugs including minocycline, apocynin, melatonin, resveratrol, quercetin, and others that act by interfering with key signaling pathways such as NF-κB, MAPK, and NOX. While this is an active therapeutic area, "inhibition of microglial activation/polarization" does not correspond to a single molecular target or receptor, but rather to a process involving multiple pathways and molecules.

Other names

Microglial activation inhibitionmicroglial polarization modulationinhibition of microglial M1 activation

Inhibition of pro-inflammatory cytokine release (e.g., TNF-α, IL-1β, IL-6) - Inhibition of NF-κB, MAPK, ERK, JAK/STAT, mTOR, or NOX signaling pathways - Promotion of anti-inflammatory (M2) polarization - Suppression of oxidative and nitrosative stress - Reduction of neurotoxic metabolite production (e.g., nitric oxide, ROS)