ArticleJournal of Huntington's disease2016
A Longitudinal Motor Characterisation of the HdhQ111 Mouse Model of Huntington's Disease.
Article in Journal of Huntington's disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed.
- Quantifying nonmnemonic strategies in two-alternative forced-choice delayed matching and nonmatching-to-position tasks in mice (Mus musculus) using automated video tracking technologies.Learning & behavior · 2026Article
- Development of cognitive, motor, metabolic, and mutant huntingtin aggregation in the zQ175 mouse model of Huntington's disease.Scientific reports · 2025Article
- From Pathogenesis to Therapeutics: A Review of 150 Years of Huntington's Disease Research.International journal of molecular sciences · 2023Review
- Motility Profile of Captive-Bred Marmosets Revealed by a Long-Term In-Cage Monitoring System.Frontiers in systems neuroscience · 2021Article
- New directions in therapeutics for Huntington disease.Future neurology · 2018Review
- The adjustment of γ-aminobutyric acidNeural regeneration research · 2018Review
- A novel ex vivo Huntington's disease model for studying GABAergic neurons and cell grafts by laser microdissection.PloS one · 2018Article
- HttQ111/+ Huntington's Disease Knock-in Mice Exhibit Brain Region-Specific Morphological Changes and Synaptic Dysfunction.Journal of Huntington's disease · 2018Article
- A selective inhibitor of histone deacetylase 3 prevents cognitive deficits and suppresses striatal CAG repeat expansions in Huntington's disease mice.Scientific reports · 2017Article
- Is there a place for human fetal-derived stem cells for cell replacement therapy in Huntington's disease?Neurochemistry international · 2017Review
- High resolution time-course mapping of early transcriptomic, molecular and cellular phenotypes in Huntington's disease CAG knock-in mice across multiple genetic backgrounds.Human molecular genetics · 2017Article
- Cognitive dysfunction in Huntington's disease: mechanisms and therapeutic strategies beyond BDNF.Brain pathology (Zurich, Switzerland) · 2016Review
- A Longitudinal Operant Assessment of Cognitive and Behavioural Changes in the HdhQ111 Mouse Model of Huntington's Disease.PloS one · 2016Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
backgroundHuntington's disease (HD) is a rare, incurable neurodegenerative disorder caused by a CAG trinucleotide expansion with the first exon of the huntingtin gene. Numerous knock-in mouse models are currently available for modelling HD. However, before their use in scientific research, these models must be characterised to determine their face and predictive validity as models of the disease and their reliability in recapitulating HD symptoms.
objectiveManifest HD is currently diagnosed upon the onset of motor symptoms, thus we sought to longitudinally characterise the progression and severity of motor signs in the HdhQ111 knock-in mouse model of HD, in heterozygous mice.
methodsAn extensive battery of motor tests including: rotarod, inverted lid test, balance beam, spontaneous locomotor activity and gait analysis were applied longitudinally to a cohort of HdhQ111 heterozygous mice in order to progressively assess motor function.
resultsA progressive failure to gain body weight was demonstrated from 11 months of age and motor problems in all measures of balance beam performance were shown in HdhQ111 heterozygous animals in comparison to wild type control animals from 9 months of age. A decreased latency to fall from the rotarod was demonstrated in HdhQ111 heterozygous animals in comparison to wild type animals, although this was not progressive with time. No genotype specific differences were demonstrated in any of the other motor tests included in the test battery.
conclusionsThe HdhQ111 heterozygous mouse demonstrates a subtle and progressive motor phenotype that begins at 9 months of age. This mouse model represents an early disease stage and would be ideal for testing therapeutic strategies that require elongated lead-in times, such as viral gene therapies or striatal transplantation.
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