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Open AccessJournal ArticleDOI

Cerebral Edema Formation After Stroke: Emphasis on Blood-Brain Barrier and the Lymphatic Drainage System of the Brain.

Sichao Chen, +2 more
- 16 Aug 2021 - 
- Vol. 15, pp 716825-716825
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TLDR
In this paper, the authors discuss how the cerebral lymphatic system participates in the formation of cerebral edema after stroke and summarize the pathophysiological process of cerebral EDema formation after stroke from the two directions of the BBB.
Abstract
Brain edema is a severe stroke complication that is associated with prolonged hospitalization and poor outcomes. Swollen tissues in the brain compromise cerebral perfusion and may also result in transtentorial herniation. As a physical and biochemical barrier between the peripheral circulation and the central nervous system (CNS), the blood-brain barrier (BBB) plays a vital role in maintaining the stable microenvironment of the CNS. Under pathological conditions, such as ischemic stroke, the dysfunction of the BBB results in increased paracellular permeability, directly contributing to the extravasation of blood components into the brain and causing cerebral vasogenic edema. Recent studies have led to the discovery of the glymphatic system and meningeal lymphatic vessels, which provide a channel for cerebrospinal fluid (CSF) to enter the brain and drain to nearby lymph nodes and communicate with the peripheral immune system, modulating immune surveillance and brain responses. A deeper understanding of the function of the cerebral lymphatic system calls into question the known mechanisms of cerebral edema after stroke. In this review, we first discuss how BBB disruption after stroke can cause or contribute to cerebral edema from the perspective of molecular and cellular pathophysiology. Finally, we discuss how the cerebral lymphatic system participates in the formation of cerebral edema after stroke and summarize the pathophysiological process of cerebral edema formation after stroke from the two directions of the BBB and cerebral lymphatic system.

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N-Acetyl-Aspartyl-Glutamate in Brain Health and Disease

TL;DR: The main effect of NAAG occurs through increased mGluR3 activation and thereby reduced glutamate release, which is a promising treatment option for many brain disorders where glutamatergic excitotoxicity plays a role.
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Microglial Activation Damages Dopaminergic Neurons through MMP-2/-9-Mediated Increase of Blood-Brain Barrier Permeability in a Parkinson’s Disease Mouse Model

TL;DR: It is suggested that microglial MMP-2/-9 activation-mediated BBB dysfunction contributed to dopaminergic neurodegeneration in rotenone-induced mouse PD model, providing a novel view for the mechanisms of Parkinsonism.
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Histone Deacetylase 3 Inhibition Decreases Cerebral Edema and Protects the Blood–Brain Barrier After Stroke

TL;DR: In this article , the effects of histone deacetylase 3 (HDAC3) inhibition on cerebral edema and blood-brain barrier (BBB) leakage and explored its underlying mechanisms.
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Glial Cells Response in Stroke

TL;DR: The therapeutic options currently being explored and developed that primarily target glial cells and can be used as neuroprotective agents for the treatment of ischemic stroke are highlighted.
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Cerebral edema after ischemic stroke: Pathophysiology and underlying mechanisms

TL;DR: This review discusses the classification and pathological characteristics of cerebral edema, the possible relationship of the development of cerebral Edema after ischemic stroke with aquaporin 4, the SUR1-TRPM4 channel, matrix metalloproteinase 9, microRNA, cerebral venous reflux, inflammatory reactions, and cerebral ischemia/reperfusion injury.
References
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Global, regional, and national life expectancy, all-cause mortality, and cause-specific mortality for 249 causes of death, 1980–2015: a systematic analysis for the Global Burden of Disease Study 2015

Haidong Wang, +844 more
- 08 Oct 2016 - 
TL;DR: The Global Burden of Disease 2015 Study provides a comprehensive assessment of all-cause and cause-specific mortality for 249 causes in 195 countries and territories from 1980 to 2015, finding several countries in sub-Saharan Africa had very large gains in life expectancy, rebounding from an era of exceedingly high loss of life due to HIV/AIDS.
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TL;DR: An anatomically distinct clearing system in the brain that serves a lymphatic-like function is described and may have relevance for understanding or treating neurodegenerative diseases that involve the mis-accumulation of soluble proteins, such as amyloid β in Alzheimer's disease.
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Structural and functional features of central nervous system lymphatic vessels

TL;DR: In searching for T-cell gateways into and out of the meninges, functional lymphatic vessels lining the dural sinuses are discovered, which may call for a reassessment of basic assumptions in neuroimmunology and sheds new light on the aetiology of neuroinflammatory and neurodegenerative diseases associated with immune system dysfunction.
Journal ArticleDOI

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TL;DR: These findings support developments of new therapeutic approaches for chronic neurodegenerative disorders directed at the blood-brain barrier and other nonneuronal cells of the neurovascular unit.
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Pericytes regulate the blood–brain barrier

TL;DR: A novel and critical role for pericytes is indicated in the integration of endothelial and astrocyte functions at the neurovascular unit, and in the regulation of the blood–brain barrier.
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How does brain edema after stroke occur?

The paper discusses how disruption of the blood-brain barrier (BBB) after stroke leads to increased permeability, allowing blood components to enter the brain and cause cerebral vasogenic edema. It also mentions the role of the glymphatic system and meningeal lymphatic vessels in the formation of cerebral edema after stroke.