http://link.springer.com/article/10.1007/s12035-017-0433-6
- Cite this article as:
- Boghdadi, A.G., Teo, L. & Bourne, J.A. Mol Neurobiol (2017). doi:10.1007/s12035-017-0433-6
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Abstract
The
limited capacity for the central nervous system (CNS) to repair itself
was first described over 100 years ago by Spanish neuroscientist Ramon
Y. Cajal. However, the exact mechanisms underlying this failure in
neuronal regeneration remain unclear and, as such, no effective
therapeutics yet exist. Numerous studies have attempted to elucidate the
biochemical and molecular mechanisms that inhibit neuronal repair with
increasing evidence suggesting that several inhibitory factors and
repulsive guidance cues active during development actually persist into
adulthood and may be contributing to the inhibition of repair. For
example, in the injured adult CNS, there are various inhibitory factors
that impede the outgrowth of neurites from damaged neurons. One of the
most potent of these neurite outgrowth inhibitors is the group of
proteins known as the myelin-associated inhibitors (MAIs), present
mainly on the membranes of oligodendroglia. Several studies have shown
that interfering with these proteins can have positive outcomes in CNS
injury models by promoting neurite outgrowth and improving functional
recovery. As such, the MAIs, their receptors, and downstream effectors
are valid drug targets for the treatment of CNS injury. This review will
discuss the current literature on MAIs in the context of CNS
development, plasticity, and injury. Molecules that interfere with the
MAIs and their receptors as potential candidates for the treatment of
CNS injury will additionally be introduced in the context of preclinical
and clinical trials.
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