Neuroprotection and its molecular mechanism following spinal cord injury

摘要: Acute spinal cord injury initiates a complex cascade of molecular events termed ‘secondary injury’, which leads to progressive degeneration ranging from early neuronal apoptosis at the lesion site delayed intact white matter tracts, and, ultimately, expansion initial injury. These secondary processes include, but are not limited to, inflammation, free radical-induced cell death, glutamate excitotoxicity, phospholipase A2 activation, and induction extrinsic intrinsic apoptotic pathways, important targets in developing neuroprotective strategies for treatment Recently, number studies have shown promising results on neuroprotection recovery function rodent models using treatments that target including manipulation PTEN-Akt/mTOR signaling pathway. The present review outlines our ongoing research mechanisms experimental briefly summarizes earlier findings therapeutic potential pharmacological