Evidence map›Paper›PMID 33370315›Full record

ArticlePloS one2020

Rapid and robust patterns of spontaneous locomotor deficits in mouse models of Huntington's disease.

Taneli Heikkinen, Timo Bragge, Niina Bhattarai, Teija Parkkari, Jukka Puoliväli, Outi Kontkanen, Patrick Sweeney, Larry C Park, Ignacio Munoz-Sanjuan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 30 citations in OpenAlex.

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  18. Dysregulation of the Basal Ganglia Indirect Pathway in Early SymptomaticThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Taneli HeikkinenCharles River Discovery Services, Kuopio, Finland.ORCID 0000-0002-8844-6618
Timo BraggeCharles River Discovery Services, Kuopio, Finland.
Niina BhattaraiSchool of Pharmacy, Faculty of Health Sciences, University of Eastern Finland, Kuopio, Finland.
Teija ParkkariCharles River Discovery Services, Kuopio, Finland.
Jukka PuoliväliCharles River Discovery Services, Kuopio, Finland.
Outi KontkanenCharles River Discovery Services, Kuopio, Finland.
Patrick SweeneyNaason Science Inc., Chungcheongbuk-do, South Korea.
Larry C ParkNaason Science Inc., Chungcheongbuk-do, South Korea.
Ignacio Munoz-SanjuanCHDI Management/CHDI Foundation, Los Angeles, California, United States of America.
CHDI Foundation · USUniversity of Eastern Finland · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is an inherited neurodegenerative disorder characterized by severe disruption of cognitive and motor functions, including changes in posture and gait. A number of HD mouse models have been engineered that display behavioral and neuropathological features of the disease, but gait alterations in these models are poorly characterized. Sensitive high-throughput tests of fine motor function and gait in mice might be informative in evaluating disease-modifying interventions. Here, we describe a hypothesis-free workflow that determines progressively changing locomotor patterns across 79 parameters in the R6/2 and Q175 mouse models of HD. R6/2 mice (120 CAG repeats) showed motor disturbances as early as at 4 weeks of age. Similar disturbances were observed in homozygous and heterozygous Q175 KI mice at 3 and 6 months of age, respectively. Interestingly, only the R6/2 mice developed forelimb ataxia. The principal components of the behavioral phenotypes produced two phenotypic scores of progressive postural instability based on kinematic parameters and trajectory waveform data, which were shared by both HD models. This approach adds to the available HD mouse model research toolbox and has a potential to facilitate the development of therapeutics for HD and other debilitating movement disorders with high unmet medical need.

Indexed as

AnimalsBiomechanical PhenomenaDisease Models, AnimalFemaleGait AnalysisHuntingtin ProteinHuntington DiseaseMaleMiceMice, TransgenicMotor ActivityMutationPostureHTT protein, humanHuntingtin Protein

Identifiers

PMID33370315
PMCPMC7769440
OpenAlexW3115630538

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.