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Brain Sciences
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Stroke 2021: Recent Advances in Stroke Neuroprotection and Repair
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Stroke 2021: Recent Advances in Stroke Neuroprotection and Repair

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neurodegenerative Diseases".

Deadline for manuscript submissions: closed (10 December 2021) | Viewed by 5294

Special Issue Editor

Dr. Arieh S Solomon

E-Mail Website
Guest Editor
Goldschleger Eye Research Institute, Tel Aviv University, Tel Aviv-Yafo, Israel
Interests: axons; central nervous system; cornea; optic nerve; eye; retina
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

The latest World Health Organization report, released in May 2018, lists the top 10 causes of death worldwide in 2016. Of the 56.9 million deaths, half (54%) were due to the top 10 causes. Occupying the first two places of the list are ischemic heart diseases and stroke, the world's leading causes of death. It is estimated that more than 15 million deaths in 2016 were due to these causes. These diseases have remained the leading causes of death globally for the last 15 years.

Stroke is not only a prominent fatal disease but also the leading cause of disability worldwide. The cruel aspect of stroke is that it leaves people with severe functional disability and/or cognitive impairment. Stroke has a great impact on the economies worldwide, as it is estimated that about 10% of the male population and 8% of the female population are handicapped. Such people need personal help in their everyday life and must be materially supported by social services.  

Understanding the pathology of stroke in all its aspects may lead to the creation of a protocol of treatment that can prevent the assault. We hope that the present Special  Issue will be of interest and value for all physicians/practitioners.

Prof. Arieh Solomon
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pathology
  • stroke
  • cognitive impairment
  • severe functional disability

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Published Papers (2 papers)

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Research

16 pages, 1094 KiB  
Article
A New NF-κB Inhibitor, MEDS-23, Reduces the Severity of Adverse Post-Ischemic Stroke Outcomes in Rats
by Elina Rubin, Agnese C. Pippione, Matthew Boyko, Giacomo Einaudi, Stefano Sainas, Massimo Collino, Carlo Cifani, Marco L. Lolli, Naim Abu-Freha, Jacob Kaplanski, Donatella Boschi and Abed N. Azab
Brain Sci. 2022, 12(1), 35; https://doi.org/10.3390/brainsci12010035 - 28 Dec 2021
Cited by 11 | Viewed by 2451
Abstract
Aim: Nuclear factor kappa B (NF-κB) is known to play an important role in the inflammatory process which takes place after ischemic stroke. The major objective of the present study was to examine the effects of MEDS-23, a potent inhibitor of NF-κB, on [...] Read more.
Aim: Nuclear factor kappa B (NF-κB) is known to play an important role in the inflammatory process which takes place after ischemic stroke. The major objective of the present study was to examine the effects of MEDS-23, a potent inhibitor of NF-κB, on clinical outcomes and brain inflammatory markers in post-ischemic stroke rats. Main methods: Initially, a Toxicity Experiment was performed to determine the appropriate dose of MEDS-23 for use in animals, as MEDS-23 was analyzed in vivo for the first time. We used the middle cerebral artery occlusion (MCAO) model for inducing ischemic stroke in rats. The effects of MEDS-23 (at 10 mg/kg, ip) on post-stroke outcomes (brain inflammation, fever, neurological deficits, mortality, and depression- and anxiety-like behaviours) was tested in several efficacy experiments. Key findings: MEDS-23 was found to be safe and significantly reduced the severity of some adverse post-stroke outcomes such as fever and neurological deficits. Moreover, MEDS-23 significantly decreased prostaglandin E2 levels in the hypothalamus and hippocampus of post-stroke rats, but did not prominently alter the levels of interleukin-6 and tumor necrosis factor-α. Significance: These results suggest that NF-κB inhibition is a potential therapeutic strategy for the treatment of ischemic stroke. Full article
(This article belongs to the Special Issue Stroke 2021: Recent Advances in Stroke Neuroprotection and Repair)
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13 pages, 1035 KiB  
Article
Insulin Resistance in Skeletal Muscle of Chronic Stroke
by Alice S. Ryan, Charlene Hafer-Macko and Heidi K. Ortmeyer
Brain Sci. 2021, 11(1), 20; https://doi.org/10.3390/brainsci11010020 - 26 Dec 2020
Cited by 1 | Viewed by 2093
Abstract
A stroke can lead to reduced mobility affecting skeletal muscle mass and fatty infiltration which could lead to systemic insulin resistance, but this has not been examined and the mechanisms are currently unknown. The objective was to compare the effects of in vivo [...] Read more.
A stroke can lead to reduced mobility affecting skeletal muscle mass and fatty infiltration which could lead to systemic insulin resistance, but this has not been examined and the mechanisms are currently unknown. The objective was to compare the effects of in vivo insulin on skeletal muscle glycogen synthase (GS) activity in paretic (P) and nonparetic (NP) skeletal muscle in chronic stroke, and to compare to nonstroke controls. Participants were mild to moderately disabled adults with chronic stroke (n = 30, 60 ± 8 years) and sedentary controls (n = 35, 62 ± 8 years). Insulin sensitivity (M) and bilateral GS activity were determined after an overnight fast and during a hyperinsulinemic-euglycemic clamp. Stroke subjects had lower aerobic capacity than controls, but M was not significantly different. Insulin-stimulated activities of GS (independent, total, fractional), as well as absolute differences (insulin minus basal) and the percent change (insulin minus basal, relative to basal) in GS activities, were all significantly lower in P versus NP muscle. Basal GS fractional activity was 3-fold higher, and the increase in GS fractional activity during the clamp was 2-fold higher in control versus P and NP muscle. Visceral fat and intermuscular fat were associated with lower M. The effect of in vivo insulin to increase GS fractional activity was associated with M in control and P muscle. A reduction in insulin action on GS in paretic muscle likely contributes to skeletal muscle-specific insulin resistance in chronic stroke. Full article
(This article belongs to the Special Issue Stroke 2021: Recent Advances in Stroke Neuroprotection and Repair)
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