A new therapy for the reduction of axon and neuron loss and promotion of axon and oligodendrocyte regeneration through inhibition of death receptor 6 pathway after ischemic cerebral stroke.
Ischemic cerebral stroke may cause disability and rehabilitation is mainly dependent on long-term exercise. However, this needs many years of consistent application. Even then, it is not certain that patients will see satisfactory recovery of function. In the ischemic stroke, disability is attributed to neuron and axon loss resulting in injury to the nervous tract. In the nerve injury model, recovery of function is dependent on axon regeneration and rewiring of the nervous tract, which may be promoted and improved through appropriate drug intervention. Death receptor 6 (DR6), a member of the tumor necrosis factor (TNF) receptor superfamily, negatively regulates neuron, axon and oligodendrocyte survival and hinders axon and oligodendrocyte regeneration. Inhibition of DR6 has shown neuroprotection in nerve injury models. We hypothesized, therefore, that pharmacological inhibition of DR6 could be beneficial to the survival of axons and neurons, the regeneration of axons and oligodendrocytes, and the improvement of neurological function after ischemic cerebral stroke.
West China School of Pharmacy, Sichuan University, Chengdu, China.
Cai-Wei
CW
Qiu
Bo
B
Sheng
Jin
J
Liu
D001369:Axons; D002545:Brain Ischemia / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008962:Models, Theoretical; D009474:Neurons / Q000166:cytology*; D009836:Oligodendroglia / Q000166:cytology*; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D020521:Stroke / Q000378:metabolism* / Q000473:pathology
D018124:Receptors, Tumor Necrosis Factor