Evidence map›Paper›PMID 27529673›Full record

ReviewBrain pathology (Zurich, Switzerland)2016

Cognitive dysfunction in Huntington's disease: mechanisms and therapeutic strategies beyond BDNF.

Mar Puigdellívol, Ana Saavedra, Esther Pérez-Navarro

Open access · greenAbstract readReview
In one paragraph

Review in Brain pathology (Zurich, Switzerland), 2016. 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
1.5field-weighted citation impact, top 19% 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, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Are Methylation Patterns in theInternational journal of molecular sciences · 2024
    Article
  8. HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Mini-symposium: Huntington's disease - introduction.Brain pathology (Zurich, Switzerland) · 2016
    Article
  19. 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

3 authors at 1 institution in 1 country.

Mar PuigdellívolDepartament de Biomedicina, Facultat de Medicina, Universitat de Barcelona, Barcelona, Catalonia, Spain.
Ana SaavedraDepartament de Biomedicina, Facultat de Medicina, Universitat de Barcelona, Barcelona, Catalonia, Spain.
Esther Pérez-NavarroDepartament de Biomedicina, Facultat de Medicina, Universitat de Barcelona, Barcelona, Catalonia, Spain.
Consorci Institut D'Investigacions Biomediques August Pi I Sunyer · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the main focuses in Huntington's disease (HD) research, as well as in most neurodegenerative diseases, is the development of new therapeutic strategies, as currently there is no treatment to delay or prevent the progression of the disease. Neuronal dysfunction and neuronal death in HD are caused by a combination of interrelated pathogenic processes that lead to motor, cognitive and psychiatric symptoms. Understanding how mutant huntingtin impacts on a plethora of cellular functions could help to identify new molecular targets. Although HD has been classically classified as a neurodegenerative disease affecting voluntary movement, lately cognitive dysfunction is receiving increased attention as it is very invalidating for patients. Thus, an ambitious goal in HD research is to find altered molecular mechanisms that contribute to cognitive decline. In this review, we have focused on those findings related to corticostriatal and hippocampal cognitive dysfunction in HD, as well as on the underlying molecular mechanisms, which constitute potential therapeutic targets. These include alterations in synaptic plasticity, transcriptional machinery and neurotrophic and neurotransmitter signaling.

Indexed as

AnimalsBrainBrain-Derived Neurotrophic FactorCognition DisordersDisease Models, AnimalGuanine Nucleotide Exchange FactorsHumansHuntington DiseaseNeural PathwaysNeuronal PlasticityProtein Serine-Threonine KinasesBrain-Derived Neurotrophic FactorGuanine Nucleotide Exchange FactorsKALRN protein, humanProtein Serine-Threonine KinasesA2ARcGMPGluN3AKalirin-7nSOCp75NTRPDEsPKA

Identifiers

PMID27529673
PMCPMC8029162
OpenAlexW2516037017

What OpenQuestion holds

Textmetadata
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.