Evidence map›Paper›PMID 24737938›Full record

ReviewExperimental neurobiology2014

Therapeutic Approaches for Inhibition of Protein Aggregation in Huntington's Disease.

Sangjune Kim, Kyong-Tai Kim

Open access · bronzeAbstract readReview
In one paragraph

Review in Experimental neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Long noncoding RNAs in ubiquitination, protein degradation, and human diseases.Biochimica et biophysica acta. Gene regulatory mechanisms · 2024
    Review
  3. Big versus small: The impact of aggregate size in disease.Protein science : a publication of the Protein Society · 2023
    Review
  4. Carbon dots as a versatile tool to monitor insulin aggregation.Analytical and bioanalytical chemistry · 2023
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Epigenetic regulation in Huntington's disease.Neurochemistry international · 2021
    Review
  10. Hearing Loss in Neurological Disorders.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Novel targets for Huntington's disease: future prospects.Degenerative neurological and neuromuscular disease · 2016
    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

2 authors at 1 institution in 1 country.

Sangjune KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Korea.
Kyong-Tai KimDepartment of Life Sciences, Pohang University of Science and Technology, Pohang 790-784, Korea. ; Division of Integrative Biosciences and Biotechnology, Pohang University of Science and Technology, Pohang 790-784, Korea.
Pohang University of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is a late-onset and progressive neurodegenerative disorder that is caused by aggregation of mutant huntingtin protein which contains expanded-polyglutamine. The molecular chaperones modulate the aggregation in early stage and known for the most potent protector of neurodegeneration in animal models of HD. Over the past decades, a number of studies have demonstrated molecular chaperones alleviate the pathogenic symptoms by polyQ-mediated toxicity. Moreover, chaperone-inducible drugs and anti-aggregation drugs have beneficial effects on symptoms of disease. Here, we focus on the function of molecular chaperone in animal models of HD, and review the recent therapeutic approaches to modulate expression and turn-over of molecular chaperone and to develop anti-aggregation drugs.

Indexed as

anti-aggregation drugHuntingtonMolecular chaperoneprotein aggregation

Identifiers

PMID24737938
PMCPMC3984955
OpenAlexW2121173687

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.