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The challenges of long-distance axon regeneration in the injured CNS

The challenges of long-distance axon regeneration in the injured CNS
The challenges of long-distance axon regeneration in the injured CNS

Injury to the central nervous system (CNS) that results in long-tract axonal damage typically leads to permanent functional deficits in areas innervated at, and below, the level of the lesion. The initial ischemia, inflammation, and neurodegeneration are followed by a progressive generation of scar tissue, dieback of transected axons, and demyelination, creating an area inhibitory to regrowth and recovery. Two ways to combat this inhibition is to therapeutically target the extrinsic and intrinsic properties of the axon-scar environment. Scar tissue within and surrounding the lesion site can be broken down using an enzyme known as chondroitinase. Negative regulators of adult neuronal growth, such as Nogo, can be neutralized with antibodies. Both therapies greatly improve functional recovery in animal models. Alternatively, modifying the intrinsic growth properties of CNS neurons through gene therapy or pharmacotherapy has also shown promising axonal regeneration after injury. Despite these promising therapies, the main challenge of long-distance axon regeneration still remains; achieving a level of functional and organized connectivity below the level of the lesion that mimics the intact CNS.

CNS regeneration, glial scar , PTEN, spinal cord injury, integrins, Nogo
0079-6123
253-294
Chew, Daniel J.
9b105524-f81d-42fd-9253-950926b5b87f
Fawcett, James W.
4549730e-9f62-45b8-820b-8a9c98d1058b
Andrews, Melissa R.
ae987a2f-878e-4ae3-a7a3-a7170712096c
Chew, Daniel J.
9b105524-f81d-42fd-9253-950926b5b87f
Fawcett, James W.
4549730e-9f62-45b8-820b-8a9c98d1058b
Andrews, Melissa R.
ae987a2f-878e-4ae3-a7a3-a7170712096c

Chew, Daniel J., Fawcett, James W. and Andrews, Melissa R. (2012) The challenges of long-distance axon regeneration in the injured CNS. Progress in Brain Research, 201, 253-294. (doi:10.1016/B978-0-444-59544-7.00013-5).

Record type: Review

Abstract

Injury to the central nervous system (CNS) that results in long-tract axonal damage typically leads to permanent functional deficits in areas innervated at, and below, the level of the lesion. The initial ischemia, inflammation, and neurodegeneration are followed by a progressive generation of scar tissue, dieback of transected axons, and demyelination, creating an area inhibitory to regrowth and recovery. Two ways to combat this inhibition is to therapeutically target the extrinsic and intrinsic properties of the axon-scar environment. Scar tissue within and surrounding the lesion site can be broken down using an enzyme known as chondroitinase. Negative regulators of adult neuronal growth, such as Nogo, can be neutralized with antibodies. Both therapies greatly improve functional recovery in animal models. Alternatively, modifying the intrinsic growth properties of CNS neurons through gene therapy or pharmacotherapy has also shown promising axonal regeneration after injury. Despite these promising therapies, the main challenge of long-distance axon regeneration still remains; achieving a level of functional and organized connectivity below the level of the lesion that mimics the intact CNS.

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More information

e-pub ahead of print date: 24 November 2012
Published date: 2012
Additional Information: Copyright © 2012 Elsevier B.V. All rights reserved.
Keywords: CNS regeneration, glial scar , PTEN, spinal cord injury, integrins, Nogo
Organisations: Biomedicine

Identifiers

Local EPrints ID: 411363
URI: https://eprints.soton.ac.uk/id/eprint/411363
ISSN: 0079-6123
PURE UUID: 882dad42-219d-405c-b173-0530b52e9694
ORCID for Melissa R. Andrews: ORCID iD orcid.org/0000-0001-5960-5619

Catalogue record

Date deposited: 19 Jun 2017 16:31
Last modified: 29 Oct 2019 01:29

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