Spinal cord injury (SCI) causes serious, chronic dysfunction which is difficult to treat. Disability, including long-lasting motor and sensory dysfunction, typically results from damage to the descending and ascending spinal tracts and interneurons and, secondarily, to the neuronal degeneration that occurs proximal and distal to the spinal insult. Numerous strategies are being implemented to protect neurons from damage, to enhance axon growth and to foster cell proliferation. Described in this report are recent clinical trials aimed at testing strategies to restore locomotion after SCI. While laboratory animal studies have indicated that it may be possible to minimize neuronal damage resulting from spinal cord injury, little progress has been made in reducing or reversing the events associated with the chronic phase of this condition. The strategy aiming to inhibit single molecule sometimes shows controversial results. In SCI, a lot of players participate in motor and sensory dysfunctions. Therefore, sufficient functional recovery may be achieved by regulating multiple targets. Regrowth of tracts connecting the brain and spinal cord, and axonal sprouting of propriospinal interneurons are fundamentally important for neuronal network working. In addition, remyelination, protection of neuronal death, inhibition of inflammation, and upregulation of beneficial influence of astrocytes are also quite crucial to supporting the axonal refining. Combination of several strategies might be useful as a practical therapy. Several compounds such as a Sema3A inhibitor, estrogen, withanoside IV and their relating compounds or other neurotrophic factor-mimicking agents may be candidates for useful SCI therapeutic drugs since those have multi-effects on damaged spinal cord. [corrected].
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