OPCs-microglia cross-talk in Alzheimer's disease: Roles and mechanisms

Alzheimer's Disease (AD) are characterized with the accumulation of hyperphosphorylated tau protein and Aβ and neuroinflammation. Disrupted myelin has been observed in the brains of AD patients before the onset of symptoms. However, it remains unknown the function of myelin-forming cells in AD pathogenesis. Oligodendrocyte precursor cells (OPCs) are the source cells of myelin-forming cells in the central nervous system (CNS). In this study, we observe an abnormally enhanced microglial phagocytosis upon in activation of autophagy in OPCs. AD transgenic mice harboring defective autophagy exhibit a remarkably decreased Aβ load while an exacerbated neurodegeneration compared to control AD mice.We propose that the enhanced microglial phagocytosis induced by the inactivation of autophagy is attributed to the neurodegeneration in AD.