scispace - formally typeset
Open AccessJournal ArticleDOI

Glymphatic System in the Central Nervous System, a Novel Therapeutic Direction Against Brain Edema After Stroke

Reads0
Chats0
TLDR
The role of the glymphatic system in the formation and regression of brain edema after stroke could promote the exclusion of fluids in the brain tissue and promote the recovery of neurological function in stroke patients as discussed by the authors.
Abstract
Stroke is the destruction of brain function and structure, and is caused by either cerebrovascular obstruction or rupture. It is a disease associated with high mortality and disability worldwide. Brain edema after stroke is an important factor affecting neurologic function recovery. The glymphatic system is a recently discovered cerebrospinal fluid (CSF) transport system. Through the perivascular space and aquaporin 4 (AQP4) on astrocytes, it promotes the exchange of CSF and interstitial fluid (ISF), clears brain metabolic waste, and maintains the stability of the internal environment within the brain. Excessive accumulation of fluid in the brain tissue causes cerebral edema, but the glymphatic system plays an important role in the process of both intake and removal of fluid within the brain. The changes in the glymphatic system after stroke may be an important contributor to brain edema. Understanding and targeting the molecular mechanisms and the role of the glymphatic system in the formation and regression of brain edema after stroke could promote the exclusion of fluids in the brain tissue and promote the recovery of neurological function in stroke patients. In this review, we will discuss the physiology of the glymphatic system, as well as the related mechanisms and therapeutic targets involved in the formation of brain edema after stroke, which could provide a new direction for research against brain edema after stroke.

read more

Content maybe subject to copyright    Report

Citations
More filters
Journal ArticleDOI

Glymphatic Dysfunction Induced Oxidative Stress and Neuro-Inflammation in Major Depression Disorders

TL;DR: In this article , the authors reviewed recent advances with regard to stress-induced glymphatic system impairment and reactive oxygen species (ROS)-mediated inflammation in major depression disorder (MDD) and showed that such impairment can lead to ROS accumulation in the microenvironment, inducing cellular injury signaling and activating NLRP3 in microglia.
Journal ArticleDOI

Glymphatic system evaluation using diffusion tensor imaging in patients with traumatic brain injury

TL;DR: The DTI-ALPS method is useful for evaluating glymphatic system impairment and quantifying its activity in patients with TBI.
Journal ArticleDOI

Improving the Function of Meningeal Lymphatic Vessels to Promote Brain Edema Absorption after Traumatic Brain Injury

TL;DR: In this article , the effects of ketoprofen, 9-cisRA, and vascular endothelial cell growth factor-C (VEGF-C) on the cerebellar medullary cistern injection of TBI rats were investigated.
Journal ArticleDOI

Dysfunctional Glymphatic System with Disrupted Aquaporin 4 Expression Pattern on Astrocytes Causes Bacterial Product Accumulation in the CSF during Pneumococcal Meningitis

TL;DR: The results clearly showed that during pneumococcal meningitis, the glymphatic system does not function because of a detachment of the astrocytic end feet from the blood-brain barrier (BBB) vascular endothelium, which leads to misplacement of AQP4 with the consequent loss of the AQP 4 water channel's functionality.
Journal ArticleDOI

Molecular, Pathological, Clinical, and Therapeutic Aspects of Perihematomal Edema in Different Stages of Intracerebral Hemorrhage

TL;DR: This review summarizes the factors that affect PHE by focusing on traditional variables, the cerebral venous drainage system, and the brain lymphatic drainage system and explains why the relationship between PHE and the functional outcome of ICH is currently controversial.
References
More filters
Journal ArticleDOI

SUR1-TRPM4 and AQP4 form a heteromultimeric complex that amplifies ion/water osmotic coupling and drives astrocyte swelling.

TL;DR: It is reported that AQP4 physically co‐assembles with the sulfonylurea receptor 1—transient receptor potential melastatin 4 (SUR1‐TRPM4) monovalent cation channel to form a novel heteromultimeric water/ion channel complex, demonstrating a novel molecular mechanism involving the SUR1‐ TRPM4‐AQP4 complex to account for bulk water influx during astrocyte swelling.
Journal ArticleDOI

Ischemic stroke and intracranial hemorrhage in glioma patients on antiangiogenic therapy

TL;DR: Overall, IS seems to be a complication of prolonged antiangiogenic therapy, while intratumoral bleeds often occur in the setting of tumor progression.
Journal ArticleDOI

Culture models to study leukocyte trafficking across the choroid plexus.

TL;DR: A porcine and human “inverted” culture insert system that enables leukocyte transmigration specifically from the physiologically relevant basolateral side and facilitates the investigation of leukocytes entry into the CNS via the blood-CSF barrier is developed.
Journal ArticleDOI

Dexmedetomidine enhances glymphatic brain delivery of intrathecally administered drugs.

TL;DR: This work shows that the clinically used α2-adrenergic agonist dexmedetomidine that enhances EEG slow-wave activity, increases brain and spinal cord drug exposure of intrathecally administered drugs in mice and rats, and demonstrates that modulation of glymphatic flow has a distinct impact on the distribution of intrathletic administered therapeutics.
Journal ArticleDOI

Neurovascular matrix metalloproteinases and the blood-brain barrier.

TL;DR: A large body of data suggests that MMPs may disrupt BBB permeability and interfere with cell-cell signaling in the neurovascular unit, and ongoing efforts are underway to validate M MPs as potential biomarkers in stroke as well as pursue MMP blockers as therapeutic opportunities.
Related Papers (5)
Trending Questions (1)
What is the association of glymphatic pathway with stroke?

The glymphatic system plays an important role in the formation and regression of brain edema after stroke, as it promotes the exchange of cerebrospinal fluid and interstitial fluid, clears brain metabolic waste, and maintains the stability of the internal environment within the brain.