Assessment of hindlimb gait as a powerful indicator of axonal loss in a murine model of progressive CNS demyelination

Dorian B. McGavern, Laurie Zoecklein, Sith Sathornsumetee, Moses Rodriguez

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Identifying the role of axonal injury in the development of permanent, irreversible neurologic disability is important to the study of central nervous system (CNS) demyelinating diseases. Our understanding of neurologic dysfunction in demyelinating diseases and the ability to assess therapeutic interventions depends on the development of objective functional assays that can non-invasively measure axonal loss. In this study, we demonstrate in a murine model of progressive CNS demyelination that assessment of the hindlimb width of stride provides a powerful indicator axonal loss and can dissociate between deficits induced by demyelination versus axonal loss. (C) 2000 Elsevier Science B.V.

Original languageEnglish (US)
Pages (from-to)396-400
Number of pages5
JournalBrain Research
Volume877
Issue number2
DOIs
StatePublished - Sep 22 2000

Fingerprint

Demyelinating Diseases
Hindlimb
Gait
Central Nervous System
Central Nervous System Diseases
Neurologic Manifestations
Nervous System
Wounds and Injuries
Therapeutics

Keywords

  • Footprint
  • Motor function
  • Multiple sclerosis
  • Neurodegeneration
  • Oligodendrocyte
  • Theiler's virus

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Assessment of hindlimb gait as a powerful indicator of axonal loss in a murine model of progressive CNS demyelination. / McGavern, Dorian B.; Zoecklein, Laurie; Sathornsumetee, Sith; Rodriguez, Moses.

In: Brain Research, Vol. 877, No. 2, 22.09.2000, p. 396-400.

Research output: Contribution to journalArticle

McGavern, Dorian B. ; Zoecklein, Laurie ; Sathornsumetee, Sith ; Rodriguez, Moses. / Assessment of hindlimb gait as a powerful indicator of axonal loss in a murine model of progressive CNS demyelination. In: Brain Research. 2000 ; Vol. 877, No. 2. pp. 396-400.
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