Immunomodulation as a neuroprotective strategy after spinal cord injury

Abstract

[Excerpt] The initial trauma to the spinal cord is just the starting point for a cascade of endogenous events that will collectively determine the injury extension. These secondary events include, but are not limited to: glutamate excitoxicity, induction of apoptotic pathways, ionic imbalances and the development of a strong and dysfunctional inflammatory response. The secondary injury is associated to an aggravation of neuronal damage increasing the extent of neurological deficits (Ek et al., 2010). The delayed secondary injury, lasting hours, days or even months, represents an attractive time-window of opportunity for neuroprotective therapeutic interventions. The main purpose of such therapies is to prevent or antagonize secondary events therefore protecting spared/surviving neural tissue and avoiding the extension of neurological impairments (Vasconcelos et al., 2016). The strong inflammatory response developed after spinal cord injury (SCI) is overall regarded as a detrimental phenomenon to recovery and has been a target for the development of therapeutics for SCI. [...]