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Life
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Motor Deficits Caused by Neurological Disorders: From Mechanism to Treatment
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Motor Deficits Caused by Neurological Disorders: From Mechanism to Treatment

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (20 September 2023) | Viewed by 2054

Special Issue Editor

Dr. Mengliang Zhang

E-Mail Website
Guest Editor
Department of Molecular Medicine, University of Southern Denmark, DK-5000 Odense, Denmark
Interests: spinal cord injury; traumatic brain injury; motor deficits; postural asymmetry; monoamine neurotransmitters

Special Issue Information

Dear Colleagues,

Motor deficits refer specifically to the effect of the damage caused to motor skills or movement provoked by many neurological disorders and conditions. These disorders and conditions include, but are not limited to, traumatic brain injury, traumatic spinal cord injury, stroke, neurodegenerative diseases, and periphery nerve injury. Neurological disorders are a predominant cause of mortality, constituting 12% of total deaths globally and consequently causing an enormous economic and social burden to  society. The symptoms of neurological disorders include a broad spectrum of motor problems, from the complete paralysis of a large part of the body, to a slight weakness in the affected muscles. Such problems affect an individual’s functioning, result in disabilities or a limitation on activities, and restrict their social activities. The aim managing motor deficits is to improve the motor skills of affected individuals, eventually cure their symptoms, and ultimately bring individuals back to their normal life. However, due to limited knowledge regarding the mechanisms that underlie these symptoms, effective treatments are lacking. Due to the complexity of injuries caused to different parts of the nervous system, plus the severity of these injuries, age, and the injury type, it is a challenge to make a correct diagnosis and thus a correct treatment regimen. Therefore, in this Special Issue, we will focus on understanding the mechanisms that underlie these motor deficits using preclinical and clinical data. Studies applying data obtained using any related disease models are welcome. In addition, any new methods for the evaluation, assessment, and treatment of motor deficits in any specific neurological disorders are equally welcome. With the knowledge collected in this Special Issue, we hope to provide some guidelines for the treatment or rehabilitation of patients suffering from certain types of neurological disorders that affect their motor functions.

Dr. Mengliang Zhang
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. Life 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 2600 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

  • neurological disorders
  • neurodegenerative diseases
  • brain injury
  • spinal cord injury
  • stroke
  • cerebral palsy
  • periphery nerve injury
  • paralysis
  • spasticity
  • contracture
  • muscle weakness
  • postural asymmetry
  • gate pattern changes
  • uncontrolled movements

Published Papers (2 papers)

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Research

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19 pages, 8165 KiB  
Article
Focal Traumatic Brain Injury Impairs the Integrity of the Basement Membrane of Hindlimb Muscle Fibers Revealed by Extracellular Matrix Immunoreactivity
by Mette Albæk Kristensen, Karen Kalhøj Rich, Tobias Christian Mogensen, Andreas Malmquist Damsgaard Jensen, Åsa Fex Svenningsen and Mengliang Zhang
Life 2024, 14(5), 543; https://doi.org/10.3390/life14050543 - 24 Apr 2024
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Abstract
Traumatic brain injury (TBI) stands as a prominent global cause of disability, with motor deficits being a common consequence. Despite its widespread impact, the precise pathological mechanisms underlying motor deficits after TBI remain elusive. In this study, hindlimb postural asymmetry (HL-PA) development [...] Read more.
Traumatic brain injury (TBI) stands as a prominent global cause of disability, with motor deficits being a common consequence. Despite its widespread impact, the precise pathological mechanisms underlying motor deficits after TBI remain elusive. In this study, hindlimb postural asymmetry (HL-PA) development in rats subjected to focal TBI was investigated to explore the potential roles of collagen IV and laminin within the extracellular matrix (ECM) of selected hindlimb muscles in the emergence of motor deficits following TBI. A focal TBI was induced by ablating the left sensorimotor cortex in rats and motor deficits were assessed by measuring HL-PA. The expression of laminin and collagen IV in eight selected muscles on each side of the hindlimbs from both TBI- and sham-operated rats were studied using immunohistochemistry and semi-quantitatively analyzed. The results indicated that the TBI rats exhibited HL-PA, characterized by flexion of the contralateral (right) hindlimb. In the sham-operated rats, the immunoreactive components of laminin and collagen IV were evenly and smoothly distributed along the border of the muscle fibers in all the investigated muscles. In contrast, in the TBI rats, the pattern was broken into aggregated, granule-like, immunoreactive components. Such a labeling pattern was detected in all the investigated muscles both from the contra- and ipsilateral sides of the TBI rats. However, in TBI rats, most of the muscles from the contralateral hindlimb showed a significantly increased expression of these two proteins in comparison with those from the ipsilateral hindlimb. In comparison to sham-operated rats, there was a significant increase in laminin and collagen IV expression in various contralateral hindlimb muscles in the TBI rats. These findings suggest potential implications of laminin and collagen IV in the development of motor deficits following a focal TBI. Full article
(This article belongs to the Special Issue Motor Deficits Caused by Neurological Disorders: From Mechanism to Treatment)
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Review

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15 pages, 952 KiB  
Review
The Role of Microglial Exosomes and miR-124-3p in Neuroinflammation and Neuronal Repair after Traumatic Brain Injury
by Ioannis Mavroudis, Ioana-Miruna Balmus, Alin Ciobica, Mircea Nicusor Nicoara, Alina Costina Luca and Dragos Octavian Palade
Life 2023, 13(9), 1924; https://doi.org/10.3390/life13091924 - 16 Sep 2023
Cited by 6 | Viewed by 1401
Abstract
(1) Background: In this study, we aimed to explore the regulatory mechanism of miR-124-3p microglial exosomes, as they were previously reported to modulate neuroinflammation and promote neuronal repair following traumatic brain injury (TBI). (2) Methods: Studies investigating the impact of microglial exosomal miRNAs, [...] Read more.
(1) Background: In this study, we aimed to explore the regulatory mechanism of miR-124-3p microglial exosomes, as they were previously reported to modulate neuroinflammation and promote neuronal repair following traumatic brain injury (TBI). (2) Methods: Studies investigating the impact of microglial exosomal miRNAs, specifically miR-124-3p, on injured neurons and brain microvascular endothelial cells (BMVECs) in the context of TBI were reviewed. (3) Results: Animal models of TBI, in vitro cell culture experiments, RNA sequencing analysis, and functional assays were employed to elucidate the mechanisms underlying the effects of miR-124-3p-loaded exosomes on neuroinflammation and neuronal repair. Anti-inflammatory M2 polarization of microglia, mTOR signaling suppression, and BMVECs-mediated autophagy were reported as the main processes contributing to neuroprotection, reduced blood-brain barrier leakage, and improved neurologic outcomes in animal models of TBI. (4) Conclusions: Microglial exosomes, particularly those carrying miR-124-3p, have emerged as promising candidates for therapeutic interventions in TBI. These exosomes exhibit neuroprotective effects, attenuate neuroinflammation, and promote neuronal repair and plasticity. However, further research is required to fully elucidate the underlying mechanisms and optimize their delivery strategies for effective treatment in human TBI cases. Full article
(This article belongs to the Special Issue Motor Deficits Caused by Neurological Disorders: From Mechanism to Treatment)
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