Interaction between Aβ and Tau in the Pathogenesis of Alzheimer's Disease

Extracellular neuritic plaques composed of amyloid-beta (A beta) protein and intracellular neurofibrillary tangles containing phosphorylated tau protein are the two hallmark proteins of Alzheimer's disease (AD), and the separate neurotoxicity of these proteins in AD has been extensively studied. However, interventions that target A beta or tau individually have not yielded substantial breakthroughs. The interest in the interactions between A beta and tau in AD is increasing, but related drug investigations are in their infancy. This review discusses how A beta accelerates tau phosphorylation and the possible mechanisms and pathways by which tau mediates A beta toxicity. This review also describes the possible synergistic effects between A beta and tau on microglial cells and astrocytes. Studies suggest that the coexistence of A beta plaques and phosphorylated tau is related to the mechanism by which A beta facilitates the propagation of tau aggregation in neuritic plaques. The interactions between A beta and tau mediate cognitive dysfunction in patients with AD. In summary, this review summarizes recent data on the interplay between A beta and tau to promote a better understanding of the roles of these proteins in the pathological process of AD and provide new insights into interventions against AD.

Automated summary

Extracellular neuritic plaques and intracellular neurofibrillary tangles, composed of amyloid-beta and phosphorylated tau protein respectively, are hallmark proteins of Alzheimer's disease. The interactions between these proteins have been extensively studied, with A beta accelerating tau phosphorylation, tau mediating A beta toxicity, and potential synergistic effects on microglial cells and astrocytes. Understanding these interactions may lead to new interventions against Alzheimer's disease.