Tau as a potential therapeutic target for ischemic stroke

Xin Chen,Hua Jiang

doi:10.18632/aging.102547

Abstract

Tau is a protein mainly expressed in adult human brain. It plays important roles both in neurodegenerative diseases and stroke. Stroke is an important cause of adult death and disability, ischemic stroke almost account for 80% in all cases. Abundant studies have proven that the increase of dysfunctional tau may act as a vital factor in pathological changes after ischemic stroke. However, the relationship between tau and ischemic stroke remains ununified. Based on present studies, we firstly introduced the structure and biological function of tau protein. Secondly, we summarized the potential regulatory mechanisms of tau protein in the process of ischemic stroke. Thirdly, we discussed about the findings in therapeutic researches of ischemic stroke. This review may be helpful in implementing new therapies for ischemic stroke and may be beneficial for the clinical and experimental studies.

Highlights

Nowadays, stroke has become the leading cause of adult disability and the second most prominent cause of death worldwide, only after coronary heart disease
This review is committed to describe the pathological roles of tau following cerebral ischemia
We provided a general aspects of tau protein, including descriptions of its structure, physiological functions and pathological functions

Summary

Introduction

Stroke has become the leading cause of adult disability and the second most prominent cause of death worldwide, only after coronary heart disease. Due to the serious tissue damage which may occur during the subsequent reperfusion (such as bleeding) and the limited therapeutic time window (within 4.5h post stroke), more than 90% of ischemic stroke patients are unavailable to intravenous t-PA therapy [2]. Previous studies mainly focused on the mechanisms of tau protein in neurodegenerative diseases [6, 7], some studies have demonstrated that increased tau immunoreactivity after brain ischemia-reperfusion injury can be observed in neuronal cells [8, 9]. We aim to update the knowledge about the genomic and proteomic changes in tau protein following ischemia/reperfusion injury and the connection between tau protein and ischemic stroke

Objectives

Findings

Conclusion