Collapsin response mediator protein-2 plays a major protective role in acute axonal degeneration

Axonal degeneration is a key pathological feature in many neurological diseases. It often leads to persistent deficits due to the inability of axons to regenerate in the central nervous system. Therefore therapeutic approaches should optimally both attenuate axonal degeneration and foster axonal reg...

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Published inNeural regeneration research Vol. 12; no. 5; pp. 692 - 695
Main Authors Zhang, Jian-Nan, Koch, Jan C
Format Journal Article
LanguageEnglish
Published India Medknow Publications and Media Pvt. Ltd 01.05.2017
Medknow Publications & Media Pvt. Ltd
Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), G?ttingen, Germany
Department of Neurology, University Medicine G?ttingen, G?ttingen, Germany
Medknow Publications & Media Pvt Ltd
Wolters Kluwer Medknow Publications
Subjects
Alzheimer's disease
Amyotrophic lateral sclerosis
Axons
Care and treatment
Cell division
Cellular proteins
collapsin response mediator protein-2; CRMP2; axonal regeneration; optic nerve cruch; axonal degeneration; calpain; axonal transport
Development and progression
Genetic aspects
Health aspects
Invited Review
Kinases
Multiple sclerosis
Neurodegenerative diseases
Optic nerve
Phosphorylation
Physiology
Proteins
Spinal cord
calpain
axonal regeneration
collapsin response mediator protein-2
CRMP2
axonal transport
axonal degeneration
optic nerve cruch
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Summary:Axonal degeneration is a key pathological feature in many neurological diseases. It often leads to persistent deficits due to the inability of axons to regenerate in the central nervous system. Therefore therapeutic approaches should optimally both attenuate axonal degeneration and foster axonal regeneration. Compelling evidence suggests that collapsin response mediator protein-2（CRMP2） might be a molecular target fulfilling these requirements. In this mini-review, we give a compact overview of the known functions of CRMP2 and its molecular interactors in neurite outgrowth and in neurodegenerative conditions. Moreover, we discuss in detail our recent findings on the role of CRMP2 in acute axonal degeneration in the optic nerve. We found that the calcium influx induced by the lesion activates the protease calpain which cleaves CRMP2, leading to impairment of axonal transport. Both calpain inhibition and CRMP2 overexpression effectively protected the proximal axons against acute axonal degeneration. Taken together, CRMP2 is further characterized as a central molecular player in acute axonal degeneration and thus evolves as a promising therapeutic target to both counteract axonal degeneration and foster axonal regeneration in neurodegenerative and neurotraumatic diseases.
Bibliography:Axonal degeneration is a key pathological feature in many neurological diseases. It often leads to persistent deficits due to the inability of axons to regenerate in the central nervous system. Therefore therapeutic approaches should optimally both attenuate axonal degeneration and foster axonal regeneration. Compelling evidence suggests that collapsin response mediator protein-2（CRMP2） might be a molecular target fulfilling these requirements. In this mini-review, we give a compact overview of the known functions of CRMP2 and its molecular interactors in neurite outgrowth and in neurodegenerative conditions. Moreover, we discuss in detail our recent findings on the role of CRMP2 in acute axonal degeneration in the optic nerve. We found that the calcium influx induced by the lesion activates the protease calpain which cleaves CRMP2, leading to impairment of axonal transport. Both calpain inhibition and CRMP2 overexpression effectively protected the proximal axons against acute axonal degeneration. Taken together, CRMP2 is further characterized as a central molecular player in acute axonal degeneration and thus evolves as a promising therapeutic target to both counteract axonal degeneration and foster axonal regeneration in neurodegenerative and neurotraumatic diseases.
collapsin response mediator protein-2; CRMP2; axonal regeneration; optic nerve cruch; axonaldegeneration; calpain; axonal transport
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Author contributions: JNZ and JCK equally wrote the manuscript, conceived and designed the work.
ISSN:1673-5374
1876-7958
DOI:10.4103/1673-5374.206631