Development of treatments targeting microglia for dementia

Abstract

Microglia are macrophage–like resident immune cells in the central nervous system (CNS). When inflammation or neuronal damage occurs in the CNS, they are activated and change their form to ameboid microglia that phagocytose and remove the unnecessary substances in the brain. Accumulation of activated microglia in and around senile plaques has been demonstrated in autopsied brains from Alzheimer's disease (AD) patients. There are various opinions about the role of microglia in AD pathology ; some believe that activated microglia contribute to the progression of AD by producing both reactive oxidative species (ROS) and proinflammatory cytokines, while others believe that they inhibit the progression of AD through the phagocytosis of amyloid–β (Aβ) and microglial dysfunction in Aβ phagocytosis increase the risk of development and progression of AD. Those opinions may suggest the complexity and variety of microglial response in AD pathology. In this manuscript, we focus on microglia as the potential target for treatment of dementia, particularly AD.