Injuries to the spinal cord result in permanent disabilities that limit daily life activities.The main reasons for these poor outcomes are the limited regenerative capacity of central neurons and the inhibitory milieu...Injuries to the spinal cord result in permanent disabilities that limit daily life activities.The main reasons for these poor outcomes are the limited regenerative capacity of central neurons and the inhibitory milieu that is established upon traumatic injuries.Despite decades of research,there is still no efficient treatment for spinal cord injury.Many strategies are tested in preclinical studies that focus on ameliorating the functional outcomes after spinal cord injury.Among these,molecular compounds are currently being used for neurological recovery,with promising results.These molecules target the axon collapsed growth cone,the inhibitory microenvironment,the survival of neurons and glial cells,and the re-establishment of lost connections.In this review we focused on molecules that are being used,either in preclinical or clinical studies,to treat spinal cord injuries,such as drugs,growth and neurotrophic factors,enzymes,and purines.The mechanisms of action of these molecules are discussed,considering traumatic spinal cord injury in rodents and humans.展开更多
Trauma to the peripheral nervous system often results in loss of motor and sensory functions of the affected area of the body,leading to a series of functional impairments(Allodi et al.,2012).Injuries to peripheral ne...Trauma to the peripheral nervous system often results in loss of motor and sensory functions of the affected area of the body,leading to a series of functional impairments(Allodi et al.,2012).Injuries to peripheral nerves initiate a series of complex events,known as Wallerian degeneration,which allows the injured axons to regenerate and reinnervate their targets(Allodi et al.,2012).Damage to a nerve induces multiple alterations,which include:axonal degeneration,breakdown of myelin sheath,Schwann cells(SC)proliferation and conversion to a repair phenotype which express cytokines and chemokines that allow the infiltration and activation of macrophages(Mietto et al.,2015;Jessen and Mirsky,2016).展开更多
基金supported by CAPESFaperj+1 种基金CNPq‘‘National Institute of Science and Technology for Regenerative Medicine”, CNPq, Brazil(to AMBM)
文摘Injuries to the spinal cord result in permanent disabilities that limit daily life activities.The main reasons for these poor outcomes are the limited regenerative capacity of central neurons and the inhibitory milieu that is established upon traumatic injuries.Despite decades of research,there is still no efficient treatment for spinal cord injury.Many strategies are tested in preclinical studies that focus on ameliorating the functional outcomes after spinal cord injury.Among these,molecular compounds are currently being used for neurological recovery,with promising results.These molecules target the axon collapsed growth cone,the inhibitory microenvironment,the survival of neurons and glial cells,and the re-establishment of lost connections.In this review we focused on molecules that are being used,either in preclinical or clinical studies,to treat spinal cord injuries,such as drugs,growth and neurotrophic factors,enzymes,and purines.The mechanisms of action of these molecules are discussed,considering traumatic spinal cord injury in rodents and humans.
文摘Trauma to the peripheral nervous system often results in loss of motor and sensory functions of the affected area of the body,leading to a series of functional impairments(Allodi et al.,2012).Injuries to peripheral nerves initiate a series of complex events,known as Wallerian degeneration,which allows the injured axons to regenerate and reinnervate their targets(Allodi et al.,2012).Damage to a nerve induces multiple alterations,which include:axonal degeneration,breakdown of myelin sheath,Schwann cells(SC)proliferation and conversion to a repair phenotype which express cytokines and chemokines that allow the infiltration and activation of macrophages(Mietto et al.,2015;Jessen and Mirsky,2016).
