engleski

Molecular and cellular mechanisms involved in the early phase of the spinal cord injury

Paralysis and disability following spinal cord injury (SCI) is among the most important challenges of modern neuroscience, since it produces lifelong dysfunctions and high medical and social costs. There are no approved pharmaceutical or medical device treatments to improve neurological outcomes following SCI today. This has prompted the search of novel technical approaches and strategies to understand the molecular changes underlying plasticity and regeneration of the spinal cord. They are going in two directions: one is to develop neuroprotective strategies to preserve neuronal networks underlying walking. Major attention is given to the “secondary injury” that is progressive self-destruction of initially unaffected spinal areas. The second approach is focusing on stem cells, which might provide trophic and immunomodulatory factors to the injured spinal cord tissue, and may, thus, enhance axonal growth and contrast neuroinflammation, with the possibility to replace dead neurons. The manipulation of endogenous spinal cord stem/progenitor cells (SPCs) represent the valid alternative to stem cell transplantation strategy, since is noninvasive and avoids the need for immune suppression of patients. The results on neonatal rat in vitro model of SCI have shown the involvement of different cell death pathways in the early phase of the SCI, suggesting the need of the simultaneous usage of different cell death pathway inhibitors to protect neuronal networks important for walking. Also, we have found the molecular marker specific for the quiescent and activated spinal cord SPCs, which allows their identification and follow up, facilitating the analysis of their (neuronal) differentiation.

spinal cord injury, endogenous spinal cord stem/progenitor cells, in vitro model

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