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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

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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

Aquaporin-4 deletion in mice reduces brain edema after acute water intoxication and ischemic stroke.

TL;DR: It is shown that mice deficient in aquaporin-4 (AQP4), a glial membrane water channel, have much better survival than wild-type mice in a model of brain edema caused by acute water intoxication, and suggested that AQP4 inhibition may provide a new therapeutic option for reducingbrain edema in a wide variety of cerebral disorders.
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Capillary pericytes regulate cerebral blood flow in health and disease

TL;DR: It is demonstrated that neuronal activity and the neurotransmitter glutamate evoke the release of messengers that dilate capillaries by actively relaxing pericytes, which are major regulators of cerebral blood flow and initiators of functional imaging signals.
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Impairment of paravascular clearance pathways in the aging brain

TL;DR: Evaluating the efficiency of CSF–ISF exchange and interstitial solute clearance is impaired in the aging brain found that bulk flow drainage via the glymphatic system is driven by cerebrovascular pulsation, and is dependent on astroglial water channels that line paravascular CSF pathways.
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Matrix Metalloproteinases and TIMPs Are Associated With Blood-Brain Barrier Opening After Reperfusion in Rat Brain

TL;DR: Brain sucrose uptake increased after 3 and 48 hours of reperfusion, with maximal opening at 48 hours and return to normal by 14 days, suggesting different mechanisms of injury for the biphasic BBB injury.
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Cerebral Arterial Pulsation Drives Paravascular CSF–Interstitial Fluid Exchange in the Murine Brain

TL;DR: It is demonstrated that cerebral arterial pulsatility is a key driver of paravascular CSF influx into and through the brain parenchyma, and suggested that changes in arterials pulsatility may contribute to accumulation and deposition of toxic solutes, including amyloid β, in the aging brain.
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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.