Fig. 7From: The neuroprotective N-terminal amyloid-β core hexapeptide reverses reactive gliosis and gliotoxicity in Alzheimer’s disease pathology modelsAstrocyte and microglia phenotypic state at increasing Aβ concentrations. Diagram depicting the change in astrocyte and microglia phenotypic state and function with increasing Aβ concentrations during AD. Astrocytes and microglia perform various neuromodulatory and neuroprotective functions in a surveillant, ‘resting’ state at low, physiological Aβ concentrations. Increasing Aβ concentrations activate astrocytes and microglia into reactive phenotypic states, inducing the production and release of various proinflammatory mediators and an increase in microglia-dependent synaptic pruning, exacerbating neuronal death. As the concentration of Aβ continues to rise during the course of AD, pathogenic Aβ levels induce cellular dysfunction, gliotoxicity, and cell death in astrocytes and microgliaBack to article page