Ischaemic stroke

Nature Reviews Disease Primers, Journal Year: 2019, Volume and Issue: 5(1)

Published: Oct. 10, 2019

Language: Английский

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Stroke

The Lancet, Journal Year: 2020, Volume and Issue: 396(10244), P. 129 - 142

Published: July 1, 2020

Language: Английский

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Inflammation and Stroke: An Overview

Neurotherapeutics, Journal Year: 2016, Volume and Issue: 13(4), P. 661 - 670

Published: Oct. 1, 2016

Language: Английский

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Signaling pathways involved in ischemic stroke: molecular mechanisms and therapeutic interventions

Signal Transduction and Targeted Therapy, Journal Year: 2022, Volume and Issue: 7(1)

Published: July 6, 2022

Abstract Ischemic stroke is caused primarily by an interruption in cerebral blood flow, which induces severe neural injuries, and one of the leading causes death disability worldwide. Thus, it great necessity to further detailly elucidate mechanisms ischemic find out new therapies against disease. In recent years, efforts have been made understand pathophysiology stroke, including cellular excitotoxicity, oxidative stress, cell processes, neuroinflammation. meantime, a plethora signaling pathways, either detrimental or neuroprotective, are also highly involved forementioned pathophysiology. These pathways closely intertwined form complex network. Also, these reveal therapeutic potential, as targeting could possibly serve approaches stroke. this review, we describe categorize them based on pathophysiological processes they participate in. Therapeutic associated with mentioned above, discussed. Meanwhile, clinical trials regarding potentially target involved, summarized details. Conclusively, review elucidated potential molecular related underlying summarize targeted various pathophysiology, particular reference future prospects for treating

Language: Английский

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Cell Death Mechanisms in Stroke and Novel Molecular and Cellular Treatment Options

Current Neuropharmacology, Journal Year: 2018, Volume and Issue: 16(9), P. 1396 - 1415

Published: March 7, 2018

As a result of ischemia or hemorrhage, blood supply to neurons is disrupted which subsequently promotes cascade pathophysiological responses resulting in cell loss. Many mechanisms are involved solely combination this disorder including excitotoxicity, mitochondrial death pathways, and the release free radicals, protein misfolding, apoptosis, necrosis, autophagy inflammation. Besides neuronal loss, damage loss astrocytes as well injury white matter contributes also cerebral injury. The core problem stroke cells makes recovery difficult even not possible late states. Acute treatment options that can be applied for mainly targeting re-establishment flow hence, their use limited due effective time window thrombolytic agents. However, if acute exceeded, starts activation pathways. This review will explore most updated cellular leading stroke. Ischemic hemorrhagic subarachnoid hemorrhage debated light novel molecular discussed.

Language: Английский

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A NeuroD1 AAV-Based Gene Therapy for Functional Brain Repair after Ischemic Injury through In Vivo Astrocyte-to-Neuron Conversion

Molecular Therapy, Journal Year: 2019, Volume and Issue: 28(1), P. 217 - 234

Published: Sept. 6, 2019

Adult mammalian brains have largely lost neuroregeneration capability except for a few niches. Previous studies converted glial cells into neurons, but the total number of neurons generated is limited and therapeutic potential unclear. Here, we demonstrate that NeuroD1-mediated in situ astrocyte-to-neuron conversion can regenerate large functional new after ischemic injury. Specifically, using NeuroD1 adeno-associated virus (AAV)-based gene therapy, were able to one third caused by injury simultaneously protect another injured leading significant neuronal recovery. RNA sequencing immunostaining confirmed recovery cell at both mRNA level protein level. Brain slice recordings found astrocyte-converted showed robust action potentials synaptic responses 2 months expression. Anterograde retrograde tracing revealed long-range axonal projections from their target regions time-dependent manner. Behavioral analyses improvement motor cognitive functions conversion. Together, these results vivo technology through NeuroD1-based therapy restore

Language: Английский

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Ultrasound treatment of neurological diseases — current and emerging applications

Nature Reviews Neurology, Journal Year: 2016, Volume and Issue: 12(3), P. 161 - 174

Published: Feb. 19, 2016

Language: Английский

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Sudden Cardiac Arrest Survivorship: A Scientific Statement From the American Heart Association

Circulation, Journal Year: 2020, Volume and Issue: 141(12)

Published: Feb. 12, 2020

Cardiac arrest systems of care are successfully coordinating community, emergency medical services, and hospital efforts to improve the process for patients who have had a cardiac arrest. As result, number people surviving sudden is increasing. However, physical, cognitive, emotional effects may linger months or years. Systematic recommendations stop short addressing partnerships needed caregivers after stabilization. This document expands resuscitation system include patients, caregivers, rehabilitative healthcare partnerships, which central survivorship.

Language: Английский

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Interleukin-1 primes human mesenchymal stem cells towards an anti-inflammatory and pro-trophic phenotype in vitro

Stem Cell Research & Therapy, Journal Year: 2017, Volume and Issue: 8(1)

Published: April 16, 2017

Inflammation is a key contributor to central nervous system (CNS) injury such as stroke, and major target for therapeutic intervention. Effective treatments CNS injuries are limited applicable only minority of patients. Stem cell-based therapies increasingly considered the treatment disease, because they can be used in-situ regulators inflammation, improve tissue repair recovery. One promising option use bone marrow-derived mesenchymal stem cells (MSCs), which secrete anti-inflammatory trophic factors, migrate towards inflamed injured sites or implanted locally. Here we tested hypothesis that pre-treatment with inflammatory cytokines prime MSCs an pro-trophic phenotype in vitro. Human from three different donors were cultured vitro treated mediators follows: interleukin (IL)-1α, IL-1β, tumour necrosis factor alpha (TNF-α) interferon-γ. After 24 h treatment, cell supernatants analysed by ELISA expression granulocyte-colony stimulating (G-CSF), IL-10, brain-derived neurotrophic (BDNF), nerve growth (NGF), IL-1 receptor antagonist (IL-1Ra) vascular endothelial (VEGF). To confirm potential MSCs, immortalised mouse microglial BV2 bacterial lipopolysaccharide (LPS) exposed conditioned media (CM) naïve IL-1-primed levels secreted microglial-derived including TNF-α, G-CSF IL-6 measured ELISA. Unstimulated constitutively expressed factors (IL-10, VEGF, BDNF, G-CSF, NGF IL-1Ra). primed IL-1α IL-1β showed increased secretion was blocked IL-1Ra. Furthermore, LPS-treated less apoptotic markers, IL-10 response CM compared unprimed MSCs. Our results demonstrate priming increases through type 1 (IL-1R1) mechanism, induces reduction LPS-activated cells. The therefore support preconditioning future therapies.

Language: Английский

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Circular RNA TLK1 Aggravates Neuronal Injury and Neurological Deficits after Ischemic Stroke via miR-335-3p/TIPARP

Journal of Neuroscience, Journal Year: 2019, Volume and Issue: 39(37), P. 7369 - 7393

Published: July 16, 2019

Circular RNAs (circRNAs) are expressed at high levels in the brain and involved various CNS diseases. However, potential role of circRNAs ischemic stroke-associated neuronal injury remains largely unknown. Here, we investigated important functions circRNA TLK1 (circTLK1) this process. The circTLK1 were significantly increased tissues a mouse model focal cerebral ischemia reperfusion. Knockdown decreased infarct volumes, attenuated injury, improved neurological deficits. Furthermore, functioned as an endogenous miR-335-3p sponge to inhibit activity, resulting increase 2,3,7,8-tetrachlorodibenzo-p-dioxin-inducible poly (ADP-ribose) polymerase expression subsequent exacerbation injury. Clinical studies confirmed plasma patients with acute stroke (59 males 12 females). Our findings reveal detrimental SIGNIFICANCE STATEMENT extent after is primary factor determining outcomes. molecular switches that control death neurons poorly understood. While our previous indicated involvement stroke, tissue isolated from animal models patients. long-term To knowledge, these results provide first definitive evidence stroke.

Language: Английский

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