Advanced Research in Neuroprotection

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 5279

Special Issue Editors


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Guest Editor
2nd Neurological University Department, Aristotle University of Thessaloniki, AHEPA General Hospital, 54634 Thessaloniki, Greece
Interests: neuroimmunology; experimental neurology; neurodegenerative diseases

E-Mail Website
Guest Editor
2nd Neurological University Department, Aristotle University of Thessaloniki, AHEPA General Hospital, 54634 Thessaloniki, Greece
Interests: neuroimmunology; experimental neurology; neurodegenerative diseases; neuropathology

Special Issue Information

Dear Colleagues,

Despite their privileged nature, the central and peripheral nervous systems may suffer injury and are vulnerable to immune attacks. Neuroinflammatory manifestations accompany alterations to the microenvironment, which may lead to neuronal dysregulation and the appearance of neurological disorders. Despite the distinct entity of each nervous system disease, they share common pathological traits, such as biochemical damage, oxidative stress, axonal loss, and neuronal death, thus revealing the essential role of neuroprotective pathways in ensuring neuronal homeostasis and longevity. Breakthroughs in the field of drug desig and neuropharmacology along with the latest progress in animal and human models have shown the utility of translational medicine, advocating for more appropriate strategies and pharmacologic agents that can mediate the task of neuroprotection.

This Special Issue, entitled “Advanced Research in Neuroprotection”, invites original research articles, short reports, and reviews that will expertly present recent advances in both experimental and clinical knowledge of neuroprotective mechanisms and strategies within various neurological disorders.

Dr. Evangelia Kesidou
Dr. Iliana Michailidou
Dr. Christos Bakirtzis
Guest Editors

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Keywords

  • neuroprotection
  • neurodegeneration
  • neuroinflammation
  • axonal loss
  • neuropharmacology
  • traumatic brain injury
  • blood–brain barrier

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Published Papers (3 papers)

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Research

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17 pages, 4098 KiB  
Article
Effects of Sildenafil on Cognitive Function Recovery and Neuronal Cell Death Protection after Transient Global Cerebral Ischemia in Gerbils
by Yeon Hee Yu, Gun Woo Kim, Yu Ran Lee, Dae-Kyoon Park, Beomjong Song and Duk-Soo Kim
Biomedicines 2024, 12(9), 2077; https://doi.org/10.3390/biomedicines12092077 - 12 Sep 2024
Cited by 2 | Viewed by 1818
Abstract
Cerebral ischemic stroke is a major cause of death worldwide due to brain cell death resulting from ischemia-reperfusion injury. However, effective treatment approaches for patients with ischemic stroke are still lacking in clinical practice. This study investigated the potential neuroprotective effects of sildenafil, [...] Read more.
Cerebral ischemic stroke is a major cause of death worldwide due to brain cell death resulting from ischemia-reperfusion injury. However, effective treatment approaches for patients with ischemic stroke are still lacking in clinical practice. This study investigated the potential neuroprotective effects of sildenafil, a phosphodiesterase-5 inhibitor, in a gerbil model of global brain ischemia. We investigated the effects of sildenafil on the expression of glial fibrillary acidic protein and aquaporin-4, which are markers related to astrocyte activation and water homeostasis, respectively. Immunofluorescence analysis showed that the number of cells co-expressing these markers, which was elevated in the ischemia-induced group, was significantly reduced in the sildenafil-treated groups. This suggests that sildenafil may have a potential mitigating effect on astrocyte activation induced by ischemia. Additionally, we performed various behavioral tests, including the open-field test, novel object recognition, Barnes maze, Y-maze, and passive avoidance tests, to evaluate sildenafil’s effect on cognitive function impaired by ischemia. Overall, the results suggest that sildenafil may serve as a neuroprotective agent, potentially alleviating delayed neuronal cell death and improving cognitive function impaired by ischemia. Full article
(This article belongs to the Special Issue Advanced Research in Neuroprotection)
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28 pages, 6856 KiB  
Article
Regulatory Role and Cytoprotective Effects of Exogenous Recombinant SELENOM under Ischemia-like Conditions and Glutamate Excitotoxicity in Cortical Cells In Vitro
by Egor A. Turovsky, Egor Y. Plotnikov and Elena G. Varlamova
Biomedicines 2024, 12(8), 1756; https://doi.org/10.3390/biomedicines12081756 - 5 Aug 2024
Cited by 1 | Viewed by 1263
Abstract
Despite the successes in the prevention and treatment of strokes, it is still necessary to search for effective cytoprotectors that can suppress the damaging factors of cerebral ischemia. Among the known neuroprotectors, there are a number of drugs with a protein nature. In [...] Read more.
Despite the successes in the prevention and treatment of strokes, it is still necessary to search for effective cytoprotectors that can suppress the damaging factors of cerebral ischemia. Among the known neuroprotectors, there are a number of drugs with a protein nature. In the present study, we were able to obtain recombinant SELENOM, a resident of the endoplasmic reticulum that exhibits antioxidant properties in its structure and functions. The resulting SELENOM was tested in two brain injury (in vitro) models: under ischemia-like conditions (oxygen-glucose deprivation/reoxygenation, OGD/R) and glutamate excitotoxicity (GluTox). Using molecular biology methods, fluorescence microscopy, and immunocytochemistry, recombinant SELENOM was shown to dose-dependently suppress ROS production in cortical cells in toxic models, reduce the global increase in cytosolic calcium ([Ca2+]i), and suppress necrosis and late stages of apoptosis. Activation of SELENOM’s cytoprotective properties occurs due to its penetration into cortical cells through actin-dependent transport and activation of the Ca2+ signaling system. The use of SELENOM resulted in increased antioxidant protection of cortical cells and suppression of the proinflammatory factors and cytokines expression. Full article
(This article belongs to the Special Issue Advanced Research in Neuroprotection)
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Review

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23 pages, 636 KiB  
Review
Identifying Biomarkers for Remyelination and Recovery in Multiple Sclerosis: A Measure of Progress
by Vito A. G. Ricigliano, Silvia Marenna, Serena Borrelli, Valentina Camera, Edgar Carnero Contentti, Natalia Szejko, Christos Bakirtzis, Sanja Gluscevic, Sara Samadzadeh, Hans-Peter Hartung, Krzysztof Selmaj, Bruno Stankoff, Giancarlo Comi and ECF Young Investigators/Fellows Initiative
Biomedicines 2025, 13(2), 357; https://doi.org/10.3390/biomedicines13020357 - 4 Feb 2025
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Abstract
Background: Multiple sclerosis (MS) pathology is characterized by acute and chronic inflammation, demyelination, axonal injury, and neurodegeneration. After decades of research into MS-related degeneration, recent efforts have shifted toward recovery and the prevention of further damage. A key area of focus is the [...] Read more.
Background: Multiple sclerosis (MS) pathology is characterized by acute and chronic inflammation, demyelination, axonal injury, and neurodegeneration. After decades of research into MS-related degeneration, recent efforts have shifted toward recovery and the prevention of further damage. A key area of focus is the remyelination process, where researchers are studying the effects of pharmacotherapy on myelin repair mechanisms. Multiple compounds are being tested for their potential to foster remyelination in different clinical settings through the application of less or more complex techniques to assess their efficacy. Objective: To review current methods and biomarkers to track myelin regeneration and recovery over time in people with MS (PwMS), with potential implications for promyelinating drug testing. Methods: Narrative review, based on a selection of PubMed articles discussing techniques to measure in vivo myelin repair and functional recovery in PwMS. Results: Non-invasive tools, such as structural Magnetic Resonance Imaging (MRI) and Positron Emission Tomography (PET), are being implemented to track myelin repair, while other techniques like evoked potentials, functional MRI, and digital markers allow the assessment of functional recovery. These methods, alone or in combination, have been employed to obtain precise biomarkers of remyelination and recovery in various clinical trials on MS. Conclusions: Combining different techniques to identify myelin restoration in MS could yield novel biomarkers, enhancing the accuracy of clinical trial outcomes for remyelinating therapies in PwMS. Full article
(This article belongs to the Special Issue Advanced Research in Neuroprotection)
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