Neuroprotection in Ischemic Stroke: From Mechanisms to Therapeutics

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 1426

Special Issue Editors


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Guest Editor
Department of Neurocience, Biomedicine and Movement Science, Università degli Studi di Verona, 37131 Verona, Italy
Interests: the link among neural plasticity, brain circuits and behavior, focusing on associative and non-associative learning in mice; neuromodulatory properties of the non-invasive brain stimulation (NIBS) techniques tDCS and rTMS in physiological and pathological conditions in mice, focusing on neural plasticity and cortical/subcortical functional networks
Institute of Medical Research, Northwestern Polytechnical University, Xi'an 710072, China
Interests: neuromodulation and neurorehabilitation for stroke, bio-signal processing; neuromusculoskeletal modeling

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Guest Editor
1. Department of Neuroscience, Università Cattolica del Sacro Cuore, Rome, Italy
2. Fondazione Policlinico Universitario A. Gemelli IRCCS, Rome, Italy
Interests: behavioral neuroscience; molecular and cellular neuroscience; neural plasticity and excitability; non-invasive brain stimulation techniques; stroke; dementia

Special Issue Information

Dear Colleagues,

Ischemic stroke is known to result in a significant loss of specific functions, mostly motor, with almost two thirds of survivors leaving the hospital with a disability. However, due to different neural and non-neural cell mechanisms (e.g. neural plasticity, glial or endothelial response), some functional aspects can be recovered. Notably, increasing evidence suggests that it is possible to effectively intervene at different timeframes with several tools, ranging from mechanical intervention to drugs, from physiotherapy to non-invasive neuromodulation. During the acute phase, a multifactorial pathological process and the causes and effects of cell death/suffering are among the main aspects to consider, while at chronic stages, interventions based on cell/network plasticity or activity modulation are mainly required.

The purpose of this Special Issue is to collect original data and reviews that focus on the mechanisms underlying neuroprotection and the recovery of brain damage in ischemic stroke, in both animal models and patients. Our hope is that contributions will give rise to a compendium, which will help to advance the knowledge of repair mechanisms and therapeutic and/or rehabilitative interventions across multiple continua to promote recovery after strokes.

Dr. Marco Cambiaghi
Dr. Le Li
Dr. Maria Vittoria Podda
Guest Editors

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Keywords

  • neural plasticity
  • neuromodulation
  • penumbra
  • quality of life
  • acute
  • chronic
  • excitotoxicity
  • molecular targets
  • clinical trials
  • safety
  • animal models
  • combination

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Published Papers (1 paper)

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Research

15 pages, 2505 KiB  
Article
The Potential Role of RANTES in Post-Stroke Therapy
by Hanna Pawluk, Renata Kołodziejska, Grzegorz Grześk, Alina Woźniak, Mariusz Kozakiewicz, Agnieszka Kosinska, Mateusz Pawluk, Magdalena Grześk-Kaczyńska, Elżbieta Grzechowiak, Jakub Wojtasik and Grzegorz Kozera
Cells 2023, 12(18), 2217; https://doi.org/10.3390/cells12182217 - 6 Sep 2023
Cited by 1 | Viewed by 1163
Abstract
One of the key response mechanisms to brain damage, that results in neurological symptoms, is the inflammatory response. It triggers processes that exacerbate neurological damage and create the right environment for the subsequent repair of damaged tissues. RANTES (Regulated upon Activation, Normal T [...] Read more.
One of the key response mechanisms to brain damage, that results in neurological symptoms, is the inflammatory response. It triggers processes that exacerbate neurological damage and create the right environment for the subsequent repair of damaged tissues. RANTES (Regulated upon Activation, Normal T Cell Expressed and Presumably Secreted) chemokine(C-C motif) ligand 5 (CCL5) is one of the chemokines that may have a dual role in stroke progression involving aggravating neuronal damage and playing an important role in angiogenesis and endothelial repair. This study concerned patients with ischemic stroke (AIS), whose CCL5 concentration was measured at various time intervals and was compared with the control group. In addition, the effect of this biomarker on neurological severity and functional prognosis was investigated. Compared to healthy patients, a higher concentration of this chemokine was demonstrated in less than 4.5 h, 24 h and on the seventh day. Differences in CCL5 levels were found to be dependent on the degree of disability and functional status assessed according to neurological scales (modified Rankin Scale, National Institutes of Health Stroke Scale). In addition, differences between various subtypes of stroke were demonstrated, and an increase in CCL5 concentration was proven to be a negative predictor of mortality in patients with AIS. The deleterious effect of CCL5 in the acute phase of stroke and the positive correlation between the tested biomarkers of inflammation were also confirmed. Full article
(This article belongs to the Special Issue Neuroprotection in Ischemic Stroke: From Mechanisms to Therapeutics)
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