Physical trauma is only part of the problem in spinal cord injury(SCI).In the days and weeks following damage,oxidative stress plays a critical role in SCI pathology.Despite years of research,conventional strategies aiming to scavenge transient free radicals have not demonstrated any clinical efficacy at curtailing oxidative stress.Evidence indicates that an aldehyde byproduct of lipid peroxidation,acrolein,is elevated following SCI,and that this species is directly toxic to neural tissues,with a much longer half-life than the better known reactive oxygen species.As both a product of,and catalyst for lipid peroxidation,acrolein induces a vicious cycle of oxidative stress,dramatically amplifying its effects,and continuously propagating degeneration in injured neuronal tissue.Extensive evidence has emerged to suggest that acrolein plays a particularly damaging role in perpetuating oxidative stress,causing cellular degeneration and functional loss in SCI.Acrolein has been shown to play a critical role in the secondary injury by contributing significantly to both motor and sensory deficits.Progress have been made to elucidate the mechanisms of acrolein-mediated damage at the cellular level and the resulting paralysis and neuropathic pain.In particular,acrolein is known to directly induce neuropathic pain in rodents through activation of the transient receptor potential ankyrin 1 receptor(TRPA1)found throughout the peripheral nervous system.Evidence suggests that acrolein may act to cause neuropathic pain following SCI by enhancing direct binding and activation of the TRPA1 receptor and propelling heightened activity of TRPA1 through persistent stimulation.Consistent with such notion,directly injection of pathological relevant acrolein into spinal cord cause motor deficits and neuropathic pain,further implicate its specific role in pathogenesis in SCI.Interestingly,an FDA-approved medication,hydralazine,has been show to lower the post-traumatic elevation of acrolein and mitigate structural and functional damage,including preserve motor function and mitigation of sensory hypersensitivity.Therefore,acrolein may be a novel therapeutic target for effective intervention,and acrolein-trapping based treatment maybe a novel therapeutic option for SCI victims.The main advantages of this therapy include clear,identifiable targets of intervention,accessible methods to monitor acrolein for early diagnosis and treatment evaluation,and available,FDA-approved acrolein-scavengers.Therefore,it is likely that anti-acrolein strategy may be a novel neuroprotective therapy in SCI that can be rapidly translated into the clinic.