ArticlePloS one2016
Quantitative Gait Analysis Using a Motorized Treadmill System Sensitively Detects Motor Abnormalities in Mice Expressing ATPase Defective Spastin.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Progressive gait and motor deficits in a rat model of Alexander disease.Behavioural brain research · 2026Article
- Photobiomodulation therapy mitigates cardiovascular aging and improves survival.Lasers in surgery and medicine · 2023Article
- TFG regulates secretory and endosomal sorting pathways in neurons to promote their activity and maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Molecular and cellular mechanisms of spastin in neural development and disease (Review).International journal of molecular medicine · 2021Review
- ESCRT-III-associated proteins and spastin inhibit protrudin-dependent polarised membrane traffic.Cellular and molecular life sciences : CMLS · 2020Article
- Article
- Complexity of Generating Mouse Models to Study the Upper Motor Neurons: Let Us Shift Focus from Mice to Neurons.International journal of molecular sciences · 2019Review
- Computer Methods for Automatic Locomotion and Gesture Tracking in Mice and Small Animals for Neuroscience Applications: A Survey.Sensors (Basel, Switzerland) · 2019Review
- Long-term imaging of dorsal root ganglia in awake behaving mice.Nature communications · 2019Article
- Hereditary spastic paraplegia: gain-of-function mechanisms revealed by new transgenic mouse.Human molecular genetics · 2019Article
- Mechanistic basis of an epistatic interaction reducing age at onset in hereditary spastic paraplegia.Brain : a journal of neurology · 2018Article
- Host genetic background influences diverse neurological responses to viral infection in mice.Scientific reports · 2017Article
- Mutant spastin proteins promote deficits in axonal transport through an isoform-specific mechanism involving casein kinase 2 activation.Human molecular genetics · 2017Article
- Defects in ER-endosome contacts impact lysosome function in hereditary spastic paraplegia.The Journal of cell biology · 2017Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The hereditary spastic paraplegias (HSPs) are genetic conditions in which there is progressive axonal degeneration in the corticospinal tract. Autosomal dominant mutations, including nonsense, frameshift and missense changes, in the gene encoding the microtubule severing ATPase spastin are the most common cause of HSP in North America and northern Europe. In this study we report quantitative gait analysis using a motorized treadmill system, carried out on mice knocked-in for a disease-associated mutation affecting a critical residue in the Walker A motif of the spastin ATPase domain. At 4 months and at one year of age homozygous mutant mice had a number of abnormal gait parameters, including in stride length and stride duration, compared to heterozygous and wild-type littermates. Gait parameters in heterozygous animals did not differ from wild-type littermates. We conclude that quantitative gait analysis using the DigiGait system sensitively detects motor abnormalities in a hereditary spastic paraplegia model, and would be a useful method for analyzing the effects of pharmacological treatments for HSP.
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