Treadmill Gait Analysis Does Not Detect Motor Deficits in Animal Models of Parkinson’s Disease or Amyotrophic Lateral Sclerosis

• Type of Material: Article
• Authors: Thomas Guillot III, Emory University; Seneshaw A. Asress, Emory University; Jason R. Richardson, Rutgers University; Jonathan D Glass, Emory University; Gary W Miller, Emory University
• Language: English
• Date: 2008-11
• Publisher: Taylor & Francis
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2008 Heldref Publications
• Final Published Version (URL): http://www.tandfonline.com/doi/abs/10.3200/JMBR.40.6.568-577?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub%3dpubmed#.U8krkKjpTic
• Title of Journal or Parent Work: Journal of Motor Behavior
• ISSN: 0022-2895
• Volume: 40
• Issue: 6
• Start Page: 568
• End Page: 577
• Keywords: SOD; motor impairment; gait analysis; amyotrophic lateral sclerosis; behavioral assessment; Parkinson’s disease; MPTP
• Research Categories: Health Sciences, Epidemiology; Health Sciences, Occupational Health and Safety; Health Sciences, Pathology

Abstract

Computerized treadmill gait analysis in models of toxicant exposure and neurodegenerative disorders holds much potential for detection and therapeutic intervention in these models, and researchers must validate the technology that assists in that data collection and analysis. The present authors used a commercially available computerized gait analysis system that used (a) a motorized treadmill on retired breeder male C57BL/6J mice, (b) the toxicant-induced (1-methyl-1-, 2-, 3-, 6-tetrahydropyridine) MPTP mouse model of Parkinson’s disease (PD), and (c) the superoxide dismutase 1 (SOD1) G93A transgenic mouse model of amyotrophic lateral sclerosis (ALS). The authors compared the detection of deficits by computerized treadmill gait analysis in MPTP-treated mice with inked-paw stride length and correlated these measures to dopamine (DA) loss. The authors found that the computerized treadmill gait analysis system did not distinguish MPTP-treated mice from vehicle controls, despite a nearly 90% deficit of striatal DA. In contrast, decreases in inked-paw stride length correlated strongly with DA losses in these same animals. Computerized treadmill gait analysis could neither reliably distinguish SOD1 G93A mutant mice from controls from 6 to 12 weeks of age nor detect any consistent early motor deficits in these mice. On the basis of the authors’ findings, they inferred that computerized gait analysis on a motorized treadmill is not suited to measuring motor deficits in either the MPTP mouse model of PD or the SOD1 G93A mouse model of ALS.