CRMPs Function in Neurons and Glial Cells: Potential Therapeutic Targets for Neurodegenerative Diseases and CNS Injury

Jun Nagai, Rina Baba, Toshio Ohshima

Research output: Contribution to journalReview articlepeer-review

12 Citations (Scopus)

Abstract

Neurodegeneration in the adult mammalian central nervous system (CNS) is fundamentally accelerated by its intrinsic neuronal mechanisms, including its poor regenerative capacity and potent extrinsic inhibitory factors. Thus, the treatment of neurodegenerative diseases faces many obstacles. The degenerative processes, consisting of axonal/dendritic structural disruption, abnormal axonal transport, release of extracellular factors, and inflammation, are often controlled by the cytoskeleton. From this perspective, regulators of the cytoskeleton could potentially be a therapeutic target for neurodegenerative diseases and CNS injury. Collapsin response mediator proteins (CRMPs) are known to regulate the assembly of cytoskeletal proteins in neurons, as well as control axonal growth and neural circuit formation. Recent studies have provided some novel insights into the roles of CRMPs in several inhibitory signaling pathways of neurodegeneration, in addition to its functions in neurological disorders and CNS repair. Here, we summarize the roles of CRMPs in axon regeneration and its emerging functions in non-neuronal cells, especially in inflammatory responses. We also discuss the direct and indirect targeting of CRMPs as a novel therapeutic strategy for neurological diseases.

Original languageEnglish
Pages (from-to)4243-4256
Number of pages14
JournalMolecular Neurobiology
Volume54
Issue number6
DOIs
Publication statusPublished - 2017 Aug 1

Keywords

  • CRMP
  • Cytoskeleton
  • Degeneration
  • Inflammation
  • Neurological diseases
  • Regeneration

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience

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