Evidence map›Paper›PMID 23936129›Full record

ArticlePloS one2013

The Q175 mouse model of Huntington's disease shows gene dosage- and age-related decline in circadian rhythms of activity and sleep.

Dawn H Loh, Takashi Kudo, Danny Truong, Yingfei Wu, Christopher S Colwell

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
–field-weighted citation impact
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

53 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Sleep Disorders in Patients with Choreic Syndromes.Current neurology and neuroscience reports · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. A Phenomenological Mouse Circadian Pacemaker Model.Journal of biological rhythms · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Circadian rhythms in neurodegenerative disorders.Nature reviews. Neurology · 2022
    Review
  17. Article
  18. Impaired Refinement of Kinematic Variability in Huntington Disease Mice on an Automated Home Cage Forelimb Motor Task.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  19. Defining circadian disruption in neurodegenerative disorders.The Journal of clinical investigation · 2021
    Review
  20. Review
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

5 authors.

Dawn H LohLaboratory of Circadian and Sleep Medicine, Department of Psychiatry and Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California, USA.
Takashi Kudo
Danny Truong
Yingfei Wu
Christopher S Colwell

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sleep and circadian disruptions are commonly reported by patients with neurodegenerative diseases, suggesting these may be an endophenotype of the disorders. Several mouse models of Huntington's disease (HD) that recapitulate the disease progression and motor dysfunction of HD also exhibit sleep and circadian rhythm disruption. Of these, the strongest effects are observed in the transgenic models with multiple copies of mutant huntingtin gene. For developing treatments of the human disease, knock-in (KI) models offer advantages of genetic precision of the insertion and control of mutation copy number. Therefore, we assayed locomotor activity and immobility-defined sleep in a new model of HD with an expansion of the KI repeats (Q175). We found evidence for gene dose- and age-dependent circadian disruption in the behavior of the Q175 line. We did not see evidence for loss of cells or disruption of the molecular oscillator in the master pacemaker, the suprachiasmatic nucleus (SCN). The combination of the precise genetic targeting in the Q175 model and the observed sleep and circadian disruptions make it tractable to study the interaction of the underlying pathology of HD and the mechanisms by which the disruptions occur.

Indexed as

Gene DosageAge FactorsAllelesAnimalsCircadian RhythmDisease Models, AnimalGenotypeHumansHuntingtin ProteinHuntington DiseaseMaleMiceMice, TransgenicMotor ActivityMutationNerve Tissue ProteinsHTT protein, humanHuntingtin ProteinNerve Tissue Proteins

Identifiers

PMID23936129
PMCPMC3728350

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.