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Topic: Pathogenesis in Spinal Cord Injury (SCI) and Therapeutic Strategies

A special issue of Neuroimmunology and Neuroinflammation

ISSN 2349-6142 (Online), ISSN 2347-8659 (Print)

Submission deadline: 30 Sep 2020

Guest Editor(s)

  • Prof. Swapan K. Ray, PhD
    Professor, Department of Pathology, Microbiology, and Immunology, University of South Carolina School of Medicine, SC, USA.

    Website | E-mail

Special Issue Introduction

Spinal cord injury (SCI) is a devastating neurological injury that mostly affects young individuals, severely limiting their normal life activities and longevity. The incidence of SCI is also significantly high in older individuals. Depending on the location of primary injury, SCI causes paraplegia or quadriplegia (also known as tetraplegia). Unfortunately, the global trend of SCI is increasing and there is yet no satisfactory treatment or cure for SCI victims. Fortunately, intense research activities are underway worldwide in order to understand the pathogenesis of SCI more clearly and to devise appropriate therapeutic strategies for prevention of progressive neurodegeneration and improvement of neurological functions in SCI patients.
Generally, SCI is classified into non-traumatic SCI and traumatic SCI based on the inducers that cause their pathogenesis. Non-traumatic injury to the spinal cord is the damage due to infection, lack of blood supply, compression caused by cancer, slow degeneration of spinal bones by osteoarthritis, vascular ischemia, multiple sclerosis, inflammatory disease, motoneuron disease, or radiation. However, most of the SCI patients all over the world are the victims of traumatic SCI that occurs due to car accidents, sporting activities, warfare, violent incidents, gunshot wounds, stabbings, and falls. The pathogenesis of traumatic SCI begins with the primary injury to the spinal cord followed by initiation of progressive secondary injury that spreads from the lesion site to the rostral and caudal areas of the spinal cord. Activation of various deleterious cellular functions, molecular factors, and signaling pathways contributes to pathogenesis in both acute and chronic traumatic SCI. Patients with acute traumatic SCI and chronic traumatic SCI suffer heavily from progressive pathogenesis and psychological problems. Therefore, traumatic SCI is the intense focus of current research for understating the cellular and molecular mechanisms of progressive pathogenesis to find out the appropriate therapeutic targets for prevention of neurodegeneration and improvement of neurological functions.
The pathogenesis in traumatic SCI involves three main programmed cell death (PCD) mechanisms: apoptosis or apoptotic cell death (type I PCD), autophagic cell death (type II PCD), and necrotic cell death (type III PCD). Apoptosis or apoptotic cell death (type I PCD) occurs due to mild to moderate extracellular or intracellular stimuli with activation of cysteine proteases (calpains and caspases). It is preventable with appropriate therapeutic interventions, at least, in animal models of traumatic SCI. Autophagy and autophagic cell death are not synonymous. Autophagy (also known as autophagocytosis) due to hypoxia or nutritional stress is a caspase-independent but cathepsin-dependent process in a cell that uses this process for lysosomal degradation of its damaged proteins, organelles, and other materials for recycling and clearing. When the metabolites or building blocks are back to the cytosol, they can be either recycled into metabolic and biosynthetic pathways or oxidized by the mitochondria to generate ATP for cell survival. However, autophagy may occur at extreme levels leading to autophagic cell death (type II PCD). The extent of autophagy and its role and contribution to cell death mechanism in traumatic SCI remain rather controversial. Manipulation of autophagy in traumatic SCI may depend on the context. Necrosis or necrotic cell death (type III PCD) is not preventable in traumatic SCI as it happens suddenly at the time of primary injury to the spinal cord and probably due to extreme insults such as intracellular oxidative stress and cytosolic Ca2+ overload during the secondary injury process.
Depending on the type and severity of traumatic SCI, current management strategies include surgery, pharmacological interventions, and rehabilitation programs. Preclinical studies involving stem cell transplantation, manipulation of microRNAs, hormonal therapeutic agents, combination of therapeutic agents, and nanodelivery of new therapeutic agents are revolutionizing the field of traumatic SCI research. These novel and innovative therapeutic strategies on the horizon are giving fresh hope of recovery to the traumatic SCI patients.
For this special issue of the journal, we are requesting submission of manuscripts that describe various mechanisms of pathogenesis in SCI and potential therapeutic strategies for successful treatment of SCI in preclinical and clinical settings.
Submissions about the following topics are welcomed:
Epidemiological trends of traumatic spinal cord injury
Neuroeconomics and treatment of traumatic spinal cord injury
Stem cell transplantation for regeneration in spinal cord injury 
Anti-inflammatory agents for treatment of spinal cord injury
Modulation of microRNA expression for neuroprotection in traumatic spinal cord injury
Steroid hormone therapy for functional recovery in spinal cord injury 
Regulation of autophagy and apoptosis for promoting neuroprotection and locomotor function in spinal cord injury
Combination therapy for increasing regeneration and functional recovery in spinal cord injury
Nanodelivery of novel therapeutic agents for spinal cord injury repair
Surgery in spinal cord injury and treatment outcomes and risk factors
Gene therapy for promoting functional outcomes after spinal cord injury in preclinical models
Current therapeutic strategies in acute and chronic spinal cord injury
Organotypic spinal cord slice culture as ex vivo model spinal cord injury for evaluating therapeutic response
Roles of reactive glial cells in neurodegenerative processes in spinal cord injury
Pathogenesis and neuroprotection in pediatric spinal cord injury
Axonal degeneration and demyelination in spinal cord injury
Physiotherapy for improving muscle strength in spinal cord injury patients
Management of neuropathic pain in spinal cord injury
Melatonin as a promising neuroprotective agent in spinal cord injury
Oligodendrogliogenesis and axonal remyelination in spinal cord injury in animals
Rehabilitation of spinal cord injury patients
Evaluation therapeutic effects of flavonoids in spinal cord injury


SCI, inflammation, cell death mechanisms, neuroprotection, stem cell transplantation, microRNAs, combination of therapeutic agents, nanodelivery

Submission Deadline

30 Sep 2020

Submission Information

For Author Instructions, please refer to http://nnjournal.net/pages/view/author_instructions
For Online Submission, please login at https://oaemesas.com/login?JournalId=nn&SpecialIssueId=240
Submission Deadline: 30 Sep 2020
Contacts: Lucia Jia, Managing Editor, [email protected]


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