Regulation of extracellular Zn2+ homeostasis in the hippocampus as a therapeutic target for Alzheimer's disease

Introduction: The hippocampus plays an important role in spatial and declarative memory. Zn2+ is released from glutamatergic (zincergic) neuron terminals in the hippocampus and serves as a signal factor. Synaptic Zn2+ homeostasis is critical for cognitive activity in the hippocampus. Amyloid-beta (A beta) is a candidate for the pathogenesis of Alzheimer's disease (AD) and interacts with Zn2+. Areas covered: This paper gives an overview of the interaction between A beta and Zn2+ in the extracellular compartment in the pathophysiology of AD. A beta is aggregated with Zn2+ and the aggregation of A beta-peptides is widely considered to be the critical step in the pathogenesis of AD. The reader will gain an understanding of recent studies on the importance of the interaction of A beta with Zn2+ in the pathophysiology and therapeutic strategy of AD. Extracellular Zn2+ in the hippocampus is a therapeutic target for AD. Expert opinion: Recent studies show that the inhibition of the interaction of A beta with extracellular Zn2+ ameliorates the pathophysiology of AD and that extracellular Zn2+ in the hippocampus is involved in transiently A beta-induced cognition deficits. Zn2+ may play as a key-mediating factor in pathophysiology in which A beta is involved and is a targeting molecule to prevent the pathogenesis of AD.