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Restoring axonal localization and transport of transmembrane receptors to promote repair within the injured CNS: a critical step in CNS regeneration

Restoring axonal localization and transport of transmembrane receptors to promote repair within the injured CNS: a critical step in CNS regeneration

作     者:Lindsey H.Forbes Melissa R.Andrews 

作者机构:School of MedicineUniversity of St.Andrews Biological SciencesUniversity of Southampton 

出 版 物:《Neural Regeneration Research》 (中国神经再生研究(英文版))

年 卷 期:2017年第12卷第1期

页      面:27-30页

核心收录:

学科分类:0710[理学-生物学] 1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100204[医学-神经病学] 10[医学] 

基  金:support from the Morton Cure Paralysis Fund and Royal Society Research grant 

主  题:axonal transport cellular therapies extracellular matrix gene therapy integrin regeneration viral vectors 

摘      要:Each neuronal subtype is distinct in how it develops,responds to environmental cues,and whether it is capable of mounting a regenerative response following *** the adult central nervous system(CNS) does not regenerate,several experimental interventions have been trialled with successful albeit limited instances of axonal *** highlight here some of these approaches including extracellular matrix(ECM) modification,cellular grafting,gene therapy-induced replacement of proteins,as well as application of *** also review the recent report demonstrating the failure of axonal localization and transport of growth-promoting receptors within certain classes of mature *** specifically,we discuss an inability of integrin receptors to localize within the axonal compartment of mature motor neurons such as in the corticospinal and rubrospinal tracts,whereas in immature neurons of those pathways and in mature sensory tracts such as in the optic nerve and dorsal column pathways these receptors readily localize within *** we assert that this failure of axonal localization contributes to the intrinsic inability of axonal *** conclude by highlighting the necessity for both combined therapies as well as a targeted approach specific to both age and neuronal subtype will be required to induce substantial CNS repair.

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