Blood-Brain Barrier Dysfunction in Mild Traumatic Brain Injury: Evidence From Preclinical Murine Models.

Yingxi Wu,Haijian Wu,Zhen Zhao,Xinying Guo,Brock Pluimer

doi:10.3389/fphys.2020.01030

Abstract

Mild traumatic brain injury (mTBI) represents more than 80% of total TBI cases and is a robust environmental risk factor for neurodegenerative diseases including Alzheimer’s disease (AD). Besides direct neuronal injury and neuroinflammation, blood–brain barrier (BBB) dysfunction is also a hallmark event of the pathological cascades after mTBI. However, the vascular link between BBB impairment caused by mTBI and subsequent neurodegeneration remains undefined. In this review, we focus on the preclinical evidence from murine models of BBB dysfunction in mTBI and provide potential mechanistic links between BBB disruption and the development of neurodegenerative diseases.

Highlights

Traumatic brain injury (TBI) is a leading cause of death and long-term disability around the world (Hackenberg and Unterberg, 2016)
Mild traumatic brain injury commonly occurs in professional sports and military service, which can be exacerbated by repetitive mild trauma injury (Baker and Patel, 2000)
We collected preclinical evidence from murine models to describe the role of blood–brain barrier (BBB) dysfunction in mild TBI (mTBI)

Summary

INTRODUCTION

Traumatic brain injury (TBI) is a leading cause of death and long-term disability around the world (Hackenberg and Unterberg, 2016). As endoplasmic reticulum stress is a key contributor to the injury-induced neurodegeneration (Oakes and Papa, 2015), the single-cell RNA sequencing data indicated that endoplasmic reticulum dysfunction in BBB may be an overlooked mechanism in mTBI Their data demonstrated that cellular interactions based on extracellular matrix of endothelial cells are heavily impacted after mTBI (Arneson et al, 2018), which is consistent with a recent report (Munji et al, 2019).

DISCUSSION

Findings

CONCLUSION