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跑步机步态分析无法检测帕金森病或肌萎缩侧索硬化症动物模型中的运动缺陷。

Treadmill gait analysis does not detect motor deficits in animal models of Parkinson's disease or amyotrophic lateral sclerosis.

作者信息

Guillot Thomas S, Asress Seneshaw A, Richardson Jason R, Glass Jonathan D, Miller Gary W

机构信息

Center for Neurodegenerative Disease, Emory University, Atlanta, GA, USA.

出版信息

J Mot Behav. 2008 Nov;40(6):568-77. doi: 10.3200/JMBR.40.6.568-577.

DOI:10.3200/JMBR.40.6.568-577
PMID:18980909
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4101085/
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.

摘要

在毒物暴露和神经退行性疾病模型中,计算机化跑步机步态分析在这些模型的检测和治疗干预方面具有很大潜力,研究人员必须验证有助于进行数据收集和分析的技术。本文作者使用了一种商用计算机化步态分析系统,该系统对(a)退休种公C57BL/6J小鼠使用电动跑步机,(b)帕金森病(PD)的毒物诱导(1-甲基-1-、2-、3-、6-四氢吡啶)MPTP小鼠模型,以及(c)肌萎缩侧索硬化症(ALS)的超氧化物歧化酶1(SOD1)G93A转基因小鼠模型进行了研究。作者比较了计算机化跑步机步态分析对MPTP处理小鼠与用墨水标记爪步幅长度检测到的缺陷,并将这些测量结果与多巴胺(DA)损失相关联。作者发现,尽管纹状体DA损失近90%,但计算机化跑步机步态分析系统无法区分MPTP处理小鼠与载体对照。相比之下,在这些相同动物中,用墨水标记爪步幅长度的减少与DA损失密切相关。计算机化跑步机步态分析既不能可靠地区分6至12周龄的SOD1 G93A突变小鼠与对照,也不能检测到这些小鼠中任何一致的早期运动缺陷。基于作者的研究结果,他们推断电动跑步机上的计算机化步态分析不适用于测量PD的MPTP小鼠模型或ALS的SOD1 G93A小鼠模型中的运动缺陷。

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The efficacy of quantitative gait analysis by the GAITRite system in evaluation of parkinsonian bradykinesia.GAITRite系统定量步态分析在评估帕金森病运动迟缓中的疗效。
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