Ischemic Stroke

Cassella, Courtney; Jagoda, Andy

doi:10.1016/j.emc.2017.07.007

Cited by 35 publications

(14 citation statements)

References 85 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…On the other hand, cognitive functions gradually deteriorate leading to dementia of Alzheimer's disease type. Presumably, in the global stroke population, the ischemia-reperfusion episodes will soon become the leading cause of death [1,6] and of the Alzheimer's disease type dementia [2,3].…”

Section: Introductionmentioning

confidence: 99%

Heterogeneity in brain distribution of activated microglia and astrocytes in a rat ischemic model of Alzheimer’s disease after 2 years of survival

Radenović

Nenadić

Ułamek-Kozioł

et al. 2020

Aging

135

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

Heterogeneity in brain distribution of activated microglia and astrocytes in a rat ischemic model of Alzheimer’s disease after 2 years of survival

Radenović

Nenadić

Ułamek-Kozioł

et al. 2020

Aging

135

View full text Add to dashboard Cite

show abstract

“…If the trend of ischemic stroke persists, about 12 million patients will die by 2030, 70 million will be after the stroke, and over 200 million disability-adjusted life-years loss will be recorded worldwide each year [4]. Thrombolysis is currently the use of choice as a treatment during ischemic stroke in humans, but thrombolysis has a limited therapeutic window and does not affect the progressive changes that develop slowly during recirculation [6]. Brain ischemia patients, as well as experimental animals develop cognitive deficits depending on survival [1][2][3][4][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Substantiation for the Use of Curcumin during the Development of Neurodegeneration after Brain Ischemia

Ułamek-Kozioł

Czuczwar

Januszewski

et al. 2020

IJMS

View full text Add to dashboard Cite

Currently available pharmacological treatment of post-ischemia-reperfusion brain injury has limited effectiveness. This review provides an assessment of the current state of neurodegeneration treatment due to ischemia-reperfusion brain injury and focuses on the role of curcumin in the diet. The purpose of this review was to provide a comprehensive overview of what was published about the benefits of curcumin influence on post-ischemic brain damage. Some data on the clinical benefits of curcumin treatment of post-ischemic brain in terms of clinical symptoms and adverse reactions have been reviewed. The data in this review contributes to a better understanding of the potential benefits of curcumin in the treatment of neurodegenerative changes after ischemia and informs scientists, clinicians, and patients, as well as their families and caregivers about the possibilities of such treatment. Due to the pleotropic properties of curcumin, including anti-amyloid, anti-tau protein hyperphosphorylation, anti-inflammatory, anti-apoptotic, and neuroprotective action, as well as increasing neuronal lifespan and promoting neurogenesis, curcumin is a promising candidate for the treatment of post-ischemic neurodegeneration with misfolded proteins accumulation. In this way, it may gain interest as a potential therapy to prevent the development of neurodegenerative changes after cerebral ischemia. In addition, it is a safe substance and inexpensive, easily accessible, and can effectively penetrate the blood–brain barrier and neuronal membranes. In conclusion, the evidence available in a review of the literature on the therapeutic potential of curcumin provides helpful insight into the potential clinical utility of curcumin in the treatment of neurological neurodegenerative diseases with misfolded proteins. Therefore, curcumin may be a promising supplementary agent against development of neurodegeneration after brain ischemia in the future. Indeed, there is a rational scientific basis for the use of curcumin for the prophylaxis and treatment of post-ischemic neurodegeneration.

show abstract

“…Ischemic stroke is a common cause of long-term disability and is the second leading cause of death worldwide. Recanalization therapy provokes cerebral ischemia/reperfusion (I/R) injury, including vascular permeability increase, blood-brain barrier (BBB) disruption, and brain edema [ 1 , 2 ]. Brain microvascular endothelial cells (BMVECs), the main cells composing the BBB, are connected by tight junction proteins such as zonula occludens 1 (ZO-1) [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Resolvin D2 protects against cerebral ischemia/reperfusion injury in rats

Zuo

Zhang

et al. 2018

Mol Brain

View full text Add to dashboard Cite

Cerebral ischemia/reperfusion (I/R) injury is a critical factor leading to a poor prognosis for ischemic stroke patients. ω-3 fatty acid supplements taken as part of a daily diet have been shown to improve the prognosis of patients with ischemic stroke. In this study, we aimed to investigate the potential effects of resolvin D2 (RvD2), a derivative of ω-3 fatty acids, and its possible advantage on cerebral I/R injury in rats. Cerebral I/R caused by middle cerebral artery occlusion and reperfusion (MCAO/R) was established in Sprague-Dawley rats. First, in rats fed a regular diet, the MCAO/R stimulus led to a significant decrease in endogenous production of RvD2. Exogenous supply of RvD2 via intraperitoneal injection reversed MCAO/R-induced brain injury, including infarction, inflammatory response, brain edema, and neurological dysfunction. Meanwhile, RvD2 reversed the MCAO/R-induced decrease in the protein level of GPR18, which has been identified as a receptor for RvD2, especially in neurons and brain microvascular endothelial cells (BMVECs). Furthermore, RvD2 exerted rescue effects on MCAO/R-induced neuron and BMVEC death. Moreover, GPR18 antagonist O-1918 could block the rescue effects of RvD2, possibly at least partially though the GPR18-ERK1/2-NOS signaling pathway. Finally, compared with ω-3 fatty acid supplements, RvD2 treatment had a better rescue effect on cerebral infarction, which may be due to the MCAO/R-induced decrease in 5-lipoxygense phosphorylation and subsequent RvD2 generation. In conclusion, compared with ω-3 fatty acids, RvD2 may be an optimal alternative and complementary treatment for ischemic stroke patients with recanalization treatment.

show abstract

Ischemic Stroke

Cited by 35 publications

References 85 publications

Heterogeneity in brain distribution of activated microglia and astrocytes in a rat ischemic model of Alzheimer’s disease after 2 years of survival

Heterogeneity in brain distribution of activated microglia and astrocytes in a rat ischemic model of Alzheimer’s disease after 2 years of survival

Substantiation for the Use of Curcumin during the Development of Neurodegeneration after Brain Ischemia

Resolvin D2 protects against cerebral ischemia/reperfusion injury in rats

Contact Info

Product

Resources

About