Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

Background: Blood-brain barrier damage has traditionally been considered to determine the occurrence and development of poststroke brain edema, a devastating and life-threatening complication. However, no treatment strategy targeting blood-brain barrier damage has been proven clinically effective in ameliorating brain edema.

Methods: In mice with stroke models induced by transient middle cerebral artery occlusion (MCAO), the changes in glymphatic system (GS) function impairment were detected by ex vivo fluorescence imaging, 2-photon in vivo imaging, and magnetic resonance imaging within 1 week after MCAO, and the effects of GS impairment and recovery on the formation and resolution of brain edema were evaluated. In addition, in patients with ischemic stroke within 1 week after onset, changes in GS function and brain edema were also observed by magnetic resonance imaging.

Results: We found that the extravasation of protein-rich fluids into the brain was not temporally correlated with edema formation after MCAO in mice, as brain edema reabsorption preceded blood-brain barrier closure. Strikingly, the time course of edema progression matched well with the GS dysfunction after MCAO. Pharmacological enhancement of the GS function significantly alleviated brain edema developed on day 2 after MCAO, accompanied by less deposition of Aβ (amyloid-β) and better cognitive function. Conversely, functional suppression of the GS delayed the absorption of brain edema on day 7 after MCAO. Moreover, patients with ischemic stroke revealed a consistent trend of GS dysfunction after reperfusion as MCAO mice, which was correlated with the severity of brain edema and functional outcomes.

Conclusions: GS is a key contributor to the formation of brain edema after ischemic stroke, and targeting the GS may be a promising strategy for treating brain edema in ischemic stroke.

Registration: URL: https://www.chictr.org.cn/showproj.html?proj=162857; Unique identifier: NFEC-2019-189.

Download full-text PDF

Source
http://dx.doi.org/10.1161/STROKEAHA.123.045941DOI Listing

Publication Analysis

Top Keywords

brain edema
40
ischemic stroke
16
brain
12
edema
12
edema ischemic
12
blood-brain barrier
12
glymphatic system
8
formation brain
8
barrier damage
8
magnetic resonance
8

Similar Publications

Cardiotoxicity remains a major clinical challenge associated with various environmental and chemotherapeutic toxicants. Sunitinib (SNB) is a potent targeted cancer drug that is reported to induce severe organ damage including renal failure. Cirsiliol (CSL) is a natural flavone that exhibits marvelous pharmacological properties.

View Article and Find Full Text PDF

Recent studies have shown that the glymphatic system plays a crucial role in driving hyperacute edema after ischemic stroke. This has sparked interest in understanding how this system changes in later phases of ischemic stroke. In this study, we utilized cisternal contrast-enhanced magnetic resonance imaging (CE-MRI) and immunofluorescence staining to investigate glymphatic system alterations at subacute and chronic phases of ischemic stroke.

View Article and Find Full Text PDF

Epithelioid glioblastoma (eGBM) is a rare subtype of glioblastoma, generally associated with a poorer prognosis than conventional GBM despite maximum resection and standard chemoradiotherapy. Here, we report a case of a 78-year-old man who presented with left hemiplegia and a well-circumscribed right frontal lobe lesion on imaging, initially suspected to be a metastatic brain tumor. Surgical resection revealed a firm, clearly demarcated mass.

View Article and Find Full Text PDF

ROSAH (retinal dystrophy, optic nerve edema, splenomegaly, anhidrosis, and headache) syndrome is a rare genetic disease caused by variants in alpha-kinase 1 (ALPK1) resulting in downstream pro-inflammatory signaling mediated by the TIFA/TRAF6/NF-κB pathway. Here, we report the design of an ALPK1 inhibitor, DF-003, with pharmacokinetic properties suitable for daily oral dosing. In biochemical assays, DF-003 potently inhibits human ALPK1 (IC = 1.

View Article and Find Full Text PDF

Purpose: This study aimed to evaluate the prognostic significance of microvessel density (MVD), assessed by CD34 immunohistochemistry (IHC), and its correlation with radiological features and bevacizumab (BEV) treatment efficacy in newly diagnosed glioblastoma.

Methods: We retrospectively analyzed 41 patients with newly diagnosed glioblastoma. MVD was quantified using CD34 IHC, and patients were stratified into low and high MVD groups according to the cutoff value determined by receiver operating characteristic curve analysis (sensitivity, 76.

View Article and Find Full Text PDF