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

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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

Paravascular pathways contribute to vasculitis and neuroinflammation after subarachnoid hemorrhage independently of glymphatic control

TL;DR: It is demonstrated that blood components rapidly enter the paravascular space following SAH and penetrate into the perivascular parenchyma throughout the brain, causing disastrous events such as cerebral vasospasm, delayed cerebral ischemia, microcirculation dysfunction and widespread periv vascular neuroinflammation.
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Reoxygenation stress on blood-brain barrier paracellular permeability and edema in the rat.

TL;DR: It is shown that H/R elicits a biphasic increase in paracellular permeability and edema, which parallel to post-stroke sequelae, despite the lack of occlusion or complete depletion of oxygen.
Journal ArticleDOI

Subarachnoid hemorrhage - Induced block of cerebrospinal fluid flow: Role of brain coagulation factor III (tissue factor).

TL;DR: It is concluded that brain TF plays an important role in localization of hemorrhage and also regulates CSF flow under normal conditions and targeting of the TF system will allow developing of new therapeutic approaches to the treatment of SAH and pathologies related toCSF flow.
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Glibenclamide Administration Attenuates Infarct Volume, Hemispheric Swelling, and Functional Impairments following Permanent Focal Cerebral Ischemia in Rats

TL;DR: Data indicate that Glib has strong neuroprotective effects following ischemic stroke and may warrant further testing in future clinical trials for human stroke.
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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.