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Biology
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Mechanisms in Neuronal Injury and Regeneration
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Mechanisms in Neuronal Injury and Regeneration

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Neuroscience".

Deadline for manuscript submissions: closed (30 January 2022) | Viewed by 3989

Special Issue Editor

Prof. Dr. Sandro Krieg

E-Mail Website
Guest Editor
Klinikum rechts der Isar, Technical University of Munich, Ismaninger Strasse 22, Munich, Germany
Interests: brain tumor; epilepsy; spine tumor; brain mapping; brain stimulation; TBI; neurosurgery; glioma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Neuronal injury can have various origins and mechanisms. From direct trauma to ischemia to tumor infiltration to toxic mediators, neuronal injury creates long-term deficits and further sequelae. While there are differences in the origin of the injury, be it an acute event or continuous neurodegeneration from tumor, inflammation or ischemia, regeneration is sparse in most cases.

This Special Issue aims to gather various treatment approaches for the reduction of neuronal injury, such as secondary mechanisms and regeneration. Regeneration can be on the neuronal and glial level, but the avoidance of secondary brain damage and the induction of functional reorganization involving other parts of the central and peripheral nervous system is also of interest.

Prof. Dr. Sandro Krieg
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. Biology 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 2700 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

  • plasticity
  • functional reorganization
  • synapse
  • brain function
  • TBI
  • brain tumor
  • glioma
  • stroke

Published Papers (2 papers)

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Research

14 pages, 1699 KiB  
Article
Neuroprotective Effects of the Inert Gas Argon on Experimental Traumatic Brain Injury In Vivo with the Controlled Cortical Impact Model in Mice
by Fritz I. Schneider, Sandro M. Krieg, Ute Lindauer, Michael Stoffel and Yu-Mi Ryang
Biology 2022, 11(2), 158; https://0-doi-org.brum.beds.ac.uk/10.3390/biology11020158 - 19 Jan 2022
Cited by 2 | Viewed by 1368
Abstract
Argon has shown neuroprotective effects after traumatic brain injury (TBI) and cerebral ischemia in vitro and in focal cerebral ischemia in vivo. The purpose of this study is to show whether argon beneficially impacts brain contusion volume (BCV) as the primary outcome parameter, [...] Read more.
Argon has shown neuroprotective effects after traumatic brain injury (TBI) and cerebral ischemia in vitro and in focal cerebral ischemia in vivo. The purpose of this study is to show whether argon beneficially impacts brain contusion volume (BCV) as the primary outcome parameter, as well as secondary outcome parameters, such as brain edema, intracranial pressure (ICP), neurological outcome, and cerebral blood flow (CBF) in an in-vivo model. Subjects were randomly assigned to either argon treatment or room air. After applying controlled cortical impact (CCI) onto the dura with 8 m/s (displacement 1 mm, impact duration 150 ms), treatment was administered by a recovery chamber with 25%, 50%, or 75% argon and the rest being oxygen for 4 h after trauma. Two control groups received room air for 15 min and 24 h, respectively. Neurological testing and ICP measurements were performed 24 h after trauma, and brains were removed to measure secondary brain damage. The primary outcome parameter, BCV, and the secondary outcome parameter, brain edema, were not significantly reduced by argon treatment at any concentration. There was a highly significant decrease in ICP at 50% argon (p = 0.001), and significant neurological improvement (beamwalk missteps) at 25% and 50% argon (p = 0.01; p = 0.049 respectively) compared to control. Full article
(This article belongs to the Special Issue Mechanisms in Neuronal Injury and Regeneration)
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17 pages, 3927 KiB  
Article
Neurotherapeutic Potential of Cervus elaphus Sibericus on Axon Regeneration and Growth Cone Reformation after H2O2-Induced Injury in Rat Primary Cortical Neurons
by Jin Young Hong, Junseon Lee, Hyunseong Kim, Wan-Jin Jeon, Changhwan Yeo, Bo Ram Choi, Jee Eun Yoon, Ji Yun Shin, Jeom-Yong Kim and In-Hyuk Ha
Biology 2021, 10(9), 833; https://0-doi-org.brum.beds.ac.uk/10.3390/biology10090833 - 26 Aug 2021
Cited by 1 | Viewed by 2034
Abstract
Cervus elaphus sibericus (CES), commonly known as deer antler, has been used as a medicinal herb because of its various pharmacological activities, including its anti-infective, anti-arthritic, anti-allergic, and anti-oxidative properties. However, the precise mechanisms by which CES functions as a potent anti-oxidative agent [...] Read more.
Cervus elaphus sibericus (CES), commonly known as deer antler, has been used as a medicinal herb because of its various pharmacological activities, including its anti-infective, anti-arthritic, anti-allergic, and anti-oxidative properties. However, the precise mechanisms by which CES functions as a potent anti-oxidative agent remain unknown; particularly, the effects of CES on cortical neurons and its neurobiological mechanism have not been examined. We used primary cortical neurons from the embryonic rat cerebral cortex and hydrogen peroxide to induce oxidative stress and damage in neurons. After post-treatment of CES at three concentrations (10, 50, and 200 µg/mL), the influence of CES on the neurobiological mechanism was assessed by immunocytochemistry, flow cytometry, and real-time PCR. CES effectively prevented neuronal death caused by hydrogen peroxide-induced damage by regulating oxidative signaling. In addition, CES significantly induced the expression of brain-derived neurotrophic factor and neurotrophin nerve growth factor, as well as regeneration-associated genes. We also observed newly processing elongated axons after CES treatment under oxidative conditions. In addition, filopodia tips generally do not form a retraction bulb, called swollen endings. Thus, CES shows therapeutic potential for treating neurological diseases by stimulating neuron repair and regeneration. Full article
(This article belongs to the Special Issue Mechanisms in Neuronal Injury and Regeneration)
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