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Open AccessJournal ArticleDOI

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

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.

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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.
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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.
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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.
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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.
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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
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Journal ArticleDOI

The Effect of Body Posture on Brain Glymphatic Transport.

TL;DR: It is proposed that the most popular sleep posture (lateral) has evolved to optimize waste removal during sleep and that posture must be considered in diagnostic imaging procedures developed in the future to assess CSF-ISF transport in humans.
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Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage.

TL;DR: The findings suggest that heme potentiates microglial activation via TLR4, in turn inducing NF-κB activation via the MyD88/TRIF signaling pathway, and ultimately increasing cytokine expression and inflammatory injury in ICH.
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Dynamic changes in water ADC, energy metabolism, extracellular space volume, and tortuosity in neonatal rat brain during global ischemia

TL;DR: Dynamic changes in the ADC of water and in the energy status were measured at postnatal day 8 or 9 in neonatal rat brains after cardiac arrest using 1H MRS/MRI and 31P MRS, indicating that cell swelling is an important cause for the ADC decrease of water.
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Glial-conditional deletion of aquaporin-4 (Aqp4) reduces blood–brain water uptake and confers barrier function on perivascular astrocyte endfeet

TL;DR: The data suggest that the blood–brain barrier (BBB) is more complex than anticipated, and under certain conditions, the astrocyte covering of brain microvessels is rate limiting to water movement.
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Brain injury after intracerebral hemorrhage: the role of thrombin and iron.

TL;DR: The role of thrombin and iron in ICH-induced injury is reviewed and it is suggested that these mechanisms may provide new therapeutic targets.
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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.