Evidence map›Paper›PMID 24795586›Full record

ReviewFrontiers in behavioral neuroscience2014

Mood disorders in Huntington's disease: from behavior to cellular and molecular mechanisms.

Patrick Pla, Sophie Orvoen, Frédéric Saudou, Denis J David, Sandrine Humbert

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in behavioral neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

33 citing papers in PubMed, 87 citations in OpenAlex.

  1. Review
  2. The pathobiology of depression in Huntington's disease: an unresolved puzzle.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. Article
  8. Morphological classification and changes in dementia (Review).Experimental and therapeutic medicine · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Observational
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
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 at 4 institutions in 1 country.

Patrick PlaInstitut Curie Orsay, France ; CNRS UMR3306 Orsay, France ; INSERM U1005 Orsay, France ; Faculté des Sciences, Université Paris-Sud Orsay, France.
Sophie OrvoenEA3544, Faculté de Pharmacie, Université Paris-Sud Châtenay-Malabry, France.
Frédéric SaudouInstitut Curie Orsay, France ; CNRS UMR3306 Orsay, France ; INSERM U1005 Orsay, France.
Denis J DavidEA3544, Faculté de Pharmacie, Université Paris-Sud Châtenay-Malabry, France.
Sandrine HumbertInstitut Curie Orsay, France ; CNRS UMR3306 Orsay, France ; INSERM U1005 Orsay, France.
Institut Curie · FRCentre National de la Recherche Scientifique · FRInstitut Galien Paris-Saclay · FRUniversité Paris-Sud · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is a neurodegenerative disorder that is best known for its effect on motor control. Mood disturbances such as depression, anxiety, and irritability also have a high prevalence in patients with HD, and often start before the onset of motor symptoms. Various rodent models of HD recapitulate the anxiety/depressive behavior seen in patients. HD is caused by an expanded polyglutamine stretch in the N-terminal part of a 350 kDa protein called huntingtin (HTT). HTT is ubiquitously expressed and is implicated in several cellular functions including control of transcription, vesicular trafficking, ciliogenesis, and mitosis. This review summarizes progress in efforts to understand the cellular and molecular mechanisms underlying behavioral disorders in patients with HD. Dysfunctional HTT affects cellular pathways that are involved in mood disorders or in the response to antidepressants, including BDNF/TrkB and serotonergic signaling. Moreover, HTT affects adult hippocampal neurogenesis, a physiological phenomenon that is implicated in some of the behavioral effects of antidepressants and is linked to the control of anxiety. These findings are consistent with the emerging role of wild-type HTT as a crucial component of neuronal development and physiology. Thus, the pathogenic polyQ expansion in HTT could lead to mood disorders not only by the gain of a new toxic function but also by the perturbation of its normal function.

Indexed as

anxietyBDNFdepressionHPA axisHuntingtinHuntington's diseaseneurogenesisserotonin

Identifiers

PMID24795586
PMCPMC4005937
OpenAlexW2157599707

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.