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

A special issue of Neuroimmunology and Neuroinflammation  (Print ISSN:2347-8659; Online ISSN:2349-6142).

Deadline for manuscript submissions: 31 Mar 2019

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Guest Editor(s)

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

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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 too. 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 in the United States and 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. So, 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 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.

Keywords:

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

Submission Information:

For Author Instructions, please refer to http://nnjournal.net/pages/view/author_instructions
For Online Submission, please login at http://www.editorialmanager.com/neurimm/default.aspx
Submission Deadline: 31 Mar 2019
Contacts: Lucia Jia, Managing Editor, editor002@nnjournal.net

 

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Neuroimmunology and Neuroinflammation ISSN 2349-6142 (Online), ISSN 2347-8659 (Print)
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