Spinal Cord Compression: Molecular, Cellular and Therapeutic Aspects

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

Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 1635

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Guest Editor
Department of Applied Chemistry, Chaoyang University of Technology, Taichung 413310, Taiwan
Interests: spinal cord injury; neuroprotection; extracellular vesicles; phytomedicine; regenerative medicine; post-operative pain
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Special Issue Information

Dear Colleagues,

Spinal cord compression could result from both atraumatic and traumatic causes. Despite the protection from the spinal vertebra, occasionally, the spinal cord is faced with an assortment of compressive forces that are caused by blood clots, neoplastic growth, infections, ectopic bone growth, or the protrusion of intervertebral discs within the restricted area of the spinal epidural space and meninges. A more drastic compression force comes from falls, traffic accidents, sports injuries, etc. To date, the only available therapy has involved drastic surgery and the systematic use of drugs, and surgery was only aided by medical examinations rather than images. The molecular and cellular study of spinal cord compression would benefit from the identification of biomarkers, which could be used as a diagnostic indication and/or a drug target for new therapies.

Efforts have been made for the molecular and cellular phenotypes of some spinal cord compression injuries, for example, cervical spondylotic myelopathy. This is the most common cause of spinal cord dysfunction, and its etiologies includes the formation of osteophytes, disc herniation, degenerative disc disease, ossification of the posterior longitudinal ligament, and pathology of ligamentum flavum. These eventually cause spinal cord compression. High-throughput methods, as well as structure-sensitive studies, have expanded our repertoire of potential biomarkers. This Special Issue of Biomedicines focuses on recent advances in the characterization of molecular and cellular events that are involved in spinal cord compression. These may provide valuable information for the diagnosis as well as treatment of the injury.

Dr. Meng-Jen Lee
Guest Editor

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Keywords

  • spinal cord compression
  • neuroprotection
  • axon regeneration
  • targets
  • oligodendrocytes
  • macrophage
  • extracellular vesicles
  • phytomedicine
  • stem cells

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Published Papers (2 papers)

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Research

17 pages, 5757 KiB  
Article
Characterization of Contusive Spinal Cord Injury by Monitoring Motor-Evoked Potential
by Angelo H. ALL, Ka-Leung Wong and Hasan A. Al-Nashash
Biomedicines 2024, 12(11), 2548; https://doi.org/10.3390/biomedicines12112548 - 7 Nov 2024
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Abstract
This study involves longitudinal neuro-electrophysiological analysis using motor-evoked potentials (MEP) and the Basso, Beattie, and Bresnahan behavioral examinations (BBB) to evaluate moderate mid-thoracic contusive spinal cord injury (SCI) in a rat model. Objectives/Background: The objective of the study is to characterize the onset [...] Read more.
This study involves longitudinal neuro-electrophysiological analysis using motor-evoked potentials (MEP) and the Basso, Beattie, and Bresnahan behavioral examinations (BBB) to evaluate moderate mid-thoracic contusive spinal cord injury (SCI) in a rat model. Objectives/Background: The objective of the study is to characterize the onset and progression of contusive SCI over an eight-week period using a clinically applicable tool in an in vivo model. The background highlights the importance of a reliable and reproducible injury model and assessment tools for SCI. Methods: The methods section describes the experimental setup, including randomly assigned rats in three groups: Sham, Control, and Injury (undergoing a moderate contusive SCI using the NYU-Impactor). MEP monitoring and BBB examinations are conducted at baseline and weekly for eight weeks post-injury. Results: The results indicate that the relative MEP power spectral decreased to 11% and 22% in the left and right hindlimbs, respectively, during the first week post-SCI. In the second week, a slight spontaneous recovery was observed, reaching 17% in the left and 31% in the right hindlimbs. Over the following four weeks post-SCI, continuing deterioration of MEP signal power was observed with no detectable recovery. Conclusions: SCI attenuates hindlimb MEP power spectral and reduces locomotion, though the changes in MEP and locomotion exhibit distinct temporal patterns. The MEP monitoring provides valuable insights into the functional integrity of motor pathways following SCI and offer a sensitive and reliable assessment. By implementing MEP monitoring, researchers can track the progression of SCI and evaluate the efficacy of therapeutic interventions quantitatively. Full article
(This article belongs to the Special Issue Spinal Cord Compression: Molecular, Cellular and Therapeutic Aspects)
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21 pages, 6758 KiB  
Article
NeuroAiDTM-II (MLC901) Promoted Neurogenesis by Activating the PI3K/AKT/GSK-3β Signaling Pathway in Rat Spinal Cord Injury Models
by Anam Anjum, Muhammad Dain Yazid, Muhammad Fauzi Daud, Jalilah Idris, Angela Min Hwei Ng, Amaramalar Selvi Naicker, Ohnmar Htwe Rashidah Ismail, Ramesh Kumar Athi Kumar and Yogeswaran Lokanathan
Biomedicines 2024, 12(8), 1920; https://doi.org/10.3390/biomedicines12081920 - 21 Aug 2024
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Abstract
Traumatic damage to the spinal cord (SCI) frequently leads to irreversible neurological deficits, which may be related to apoptotic neurodegeneration in nerve tissue. The MLC901 treatment possesses neuroprotective and neuroregenerative activity. This study aimed to explore the regenerative potential of MLC901 and the [...] Read more.
Traumatic damage to the spinal cord (SCI) frequently leads to irreversible neurological deficits, which may be related to apoptotic neurodegeneration in nerve tissue. The MLC901 treatment possesses neuroprotective and neuroregenerative activity. This study aimed to explore the regenerative potential of MLC901 and the molecular mechanisms promoting neurogenesis and functional recovery after SCI in rats. A calibrated forceps compression injury for 15 s was used to induce SCI in rats, followed by an examination of the impacts of MLC901 on functional recovery. The Basso, Beattie, and Bresnahan (BBB) scores were utilized to assess neuronal functional recovery; H&E and immunohistochemistry (IHC) staining were also used to observe pathological changes in the lesion area. Somatosensory Evoked Potentials (SEPs) were measured using the Nicolet® Viking Quest™ apparatus. Additionally, we employed the Western blot assay to identify PI3K/AKT/GSK-3β pathway-related proteins and to assess the levels of GAP-43 and GFAP through immunohistochemistry staining. The study findings revealed that MLC901 improved hind-limb motor function recovery, alleviating the pathological damage induced by SCI. Moreover, MLC901 significantly enhanced locomotor activity, SEPs waveform, latency, amplitude, and nerve conduction velocity. The treatment also promoted GAP-43 expression and reduced reactive astrocytes (GFAP). MLC901 treatment activated p-AKT reduced p-GSK-3β expression levels and showed a normalized ratio (fold changes) relative to β-tubulin. Specifically, p-AKT exhibited a 4-fold increase, while p-GSK-3β showed a 2-fold decrease in T rats compared to UT rats. In conclusion, these results suggest that the treatment mitigates pathological tissue damage and effectively improves neural functional recovery following SCI, primarily by alleviating apoptosis and promoting neurogenesis. The underlying molecular mechanism of this treatment mainly involves the activation of the PI3K/AKT/GSK-3β pathway. Full article
(This article belongs to the Special Issue Spinal Cord Compression: Molecular, Cellular and Therapeutic Aspects)
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