Molecular mechanisms of microglial response in response to amyloid–β accumulation

Abstract

Alzheimer disease (AD) research began with the neuropathology of autopsy brains and progressed dramatically from biochemical studies to genetics and molecular biology studies of familial AD. Amyloid–β (Aβ) and tau proteins, which are major components of senile plaques and neurofibrillary tangles, respectively, play an important role in the pathogenic process. Pathologically, the activation of glial cells has been thought to be a result of the appearance of these abnormal protein accumulations or neurodegeneration. However, several genetic analyses of sporadic AD have revealed that glial cells, especially microglia, play an important role in the pathogenesis of AD. The development of antibody drugs such as Aducanumab has also highlighted the therapeutic potential of microglia in the treatment of AD. In this article, we discuss recent findings on microglia in AD.