Advances in Research on Spinal Cord Injury
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: closed (20 October 2021) | Viewed by 25506
Special Issue Editors
Interests: Calpain; inflammation; demyelination; neurodegeneration; multiple sclerosis; optic neuritis; Parkinsonson’s disease; spinal cord injury
Special Issue Information
Dear Colleagues,
Spinal cord injury (SCI) is one of the most devastating of all traumatic events, resulting in a loss or impairment of function causing reduced mobility or sensation. While the primary injury results from external mechanical forces at the injury site leading to irreversible necrotic cell death and tissue destruction, devastating secondary injury processes continue to cause damage to tissue below the lesion. The secondary injury involves multiple cellular and molecular events such as ischemia, edema, excitotoxicity, inflammation, electrolyte imbalance, free radical damage, increased proteinases and lipases, and apoptosis. Blood vessel disruption due to the initial primary injury may also lead to edema and ischemia, triggering a secondary injury cascade that causes further damage to axons and contributes to neuronal death, which may be preventable with early intervention. Interestingly, recent discoveries have shown some promising results on the induction of neuroprotection and recovery of function in animal models of SCI that may be targeted for novel therapies. Neurological deficits in SCI are visible following neuronal and myelinated axonal degeneration in people with SCI, who often experience loss of bladder function, motor impairment, and paralysis. Thus, it is apparent that the neuroplasticity of spinal circuitry underlies some functional recovery which represents a therapeutic target to improve locomotor function after SCI. However, the cellular and molecular mechanisms mediating neuroplasticity below the lesion level are not clearly understood, although some studies have focused on the mechanisms causing paralysis after SCI. Among the treatment possibilities discussed are cell transplantation strategies, including the use of fetal spinal cord tissue, remyelination in SCI models, and high-dose steroid therapy immediately after SCI. However, no single effective pharmacotherapeutic agent has been available to attenuate these destructive processes to improve function. Although advances have been made toward understanding the complex molecular mechanisms involved in SCI, a number of agents (methylprednisolone, gacyclidine, etc.) used off-label have been found ineffective for the treatment of SCI. Many therapeutic strategies have also been proposed to overcome neurodegenerative events and attenuate secondary neuronal damage. Despite the recent advances made in SCI research, much remains to be learned to ameliorate dysfunction and disability caused by SCI. This Special Issue is focused on “Advances in Research on Spinal Cord Injury”, with the goal of evaluating the role of cellular and molecular bases in the pathophysiology of spinal cord injury. The scope of this Issue also includes molecular mechanisms of neuroprotection in SCI and summarizes recent findings on the therapeutic and translational potential of pharmacological agents in SCI.
Prof. Dr. Naren L. Banik
Dr. Azizul Haque
Guest Editors
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Keywords
- spinal cord injury
- gliosis
- neurodegeneration
- axonal damage
- paralysis
- regeneration
- neuroprotection
- locomotor function
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