Stroke-induced damage on the blood–brain barrier

Well we've known about this for over a decade. Why didn't your incompetent mentors and senior researchers tell you to do the research to solve this by preventing the problem from occurring? 

Inflammatory action leaking through the blood brain barrier. May 2013

The latest incompetent shit here:

Stroke-induced damage on the blood–brain barrier

Song Xue Xin Zhou Zhi-Hui Yang Xiang-Kun Si Xin Sun^*

• Stroke Center, Department of Neurology, The First Hospital of Jilin University, Changchun, China

The blood–brain barrier (BBB) is a functional phenotype exhibited by the neurovascular unit (NVU). It is maintained and regulated by the interaction between cellular and non-cellular matrix components of the NVU. The BBB plays a vital role in maintaining the dynamic stability of the intracerebral microenvironment as a barrier layer at the critical interface between the blood and neural tissues. The large contact area (approximately 20 m²/1.3 kg brain) and short diffusion distance between neurons and capillaries allow endothelial cells to dominate the regulatory role. The NVU is a structural component of the BBB. Individual cells and components of the NVU work together to maintain BBB stability. One of the hallmarks of acute ischemic stroke is the disruption of the BBB, including impaired function of the tight junction and other molecules, as well as increased BBB permeability, leading to brain edema and a range of clinical symptoms. This review summarizes the cellular composition of the BBB and describes the protein composition of the barrier functional junction complex and the mechanisms regulating acute ischemic stroke-induced BBB disruption.

1. Introduction

Proper central nervous system (CNS) functioning requires a highly specific and dynamically stable intracerebral microenvironment with extremely high metabolic demands and dependence on electrical and chemical signals for transmitting and processing neural information. Therefore, the cerebral vasculature has a unique structural function as the blood–brain barrier (BBB). The structural basis of the BBB is microvascular endothelial cells, which, with astrocytes, basement membranes, pericytes, and neurons that are physically close to the endothelium, form the neurovascular unit (NVU). The corresponding cells, the accompanying junction complexes, and transport proteins constitute three main functions of the BBB: physical, transport, and metabolic barriers. These barriers strictly control the entry of water molecules, ions, proteins, lipids, and cells from the blood into brain tissues and promptly discharge and degrade metabolites or harmful substances in brain tissues to maintain brain microenvironment homeostasis and normal neurological functions. Ischemic stroke structurally and functionally disrupts the barrier function of the NVU, leading to BBB leakage and triggering a range of clinical symptoms. This review first deals with the interactions of BBB-related cell types/structures (endothelial cells, glial cells, pericytes, neurons, and extracellular matrix) in the NVU. This summary outlines the changes that occur during BBB disruption in ischemic stroke and the main regulatory mechanisms. Understanding normal BBB function and post-infarction changes in the BBB will help evaluate and treat ischemic stroke in the future.

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