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Anti‐ N ogo‐ A antibody: a treatment option for neurogenic lower urinary tract dysfunction?
Author(s) -
Schneider Marc P.,
Schwab Martin E.,
Kessler Thomas M.
Publication year - 2015
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/bju.13007
Subject(s) - neurite , multiple sclerosis , growth cone , myelin , microbiology and biotechnology , antibody , corticospinal tract , spinal cord injury , neuroprotection , monoclonal antibody , in vivo , axon , medicine , neuroscience , chemistry , in vitro , pharmacology , biology , immunology , spinal cord , central nervous system , biochemistry , radiology , diffusion mri , magnetic resonance imaging
In the late 1980s, Caroni and Schwab [1] showed that the myelin membrane of oligodendrocytes inhibited nerve fibre growth in the CNS. A monoclonal IgM antibody against an unknown CNS myelin protein later known as Nogo-A induced substantial axonal sprouting and functional recovery in vitro and in vivo. Nowadays, the responsible neurite growth inhibitory surface protein, Nogo-A, and its receptors NgR1 and S1PR2 have been identified and well-studied [2,3]. Nogo-A destabilises the cytoskeleton via the rho/rho-associated protein kinase (ROCK) pathway causing growth cone collapse and inhibiting neuronal growth and plasticity by down-regulation of growth-associated genes. Nogo-A suppression or neutralisation leads to an increase in sprouting, axonal regeneration and neuronal plasticity and thereby to greater functional recovery after different types of CNS injuries.