Evidence map›Paper›PMID 28339401›Full record

ReviewJournal of Huntington's disease2017

Is Huntingtin Dispensable in the Adult Brain?

Jeh-Ping Liu, Scott O Zeitlin

Abstract readReview
In one paragraph

Review in Journal of Huntington's disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 46 citations in OpenAlex.

  1. Structural-functional analyses of the huntingtin/HAP40 complex inJournal of biomolecular structure & dynamics · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Huntington's Disease: Complex Pathogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Review
  20. Histone deacetylase-3: Friend and foe of the brain.Experimental biology and medicine (Maywood, N.J.) · 2020
    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.

Jeh-Ping Liu
Scott O Zeitlin
University of Virginia · US

Funding

Huntingtin proline-rich region modulation of Huntington's disease pathogenesisR01NS077926 · NINDS · UNIVERSITY OF VIRGINIA · PI ZEITLIN, SCOTT · 2014 to 2018
$1.7M
Modeling the effects of reducing huntingtin and Hdh alternative splicing in miceR01NS090914 · NINDS · UNIVERSITY OF VIRGINIA · PI ZEITLIN, SCOTT · 2015 to 2018
$1.4M
NINDS NIH HHS R01 NS077926NINDS NIH HHS R01 NS090914
6 · The paper itself

Abstract

Huntingtin (HTT) is an essential protein during early embryogenesis and the development of the central nervous system (CNS). Conditional knock-out of mouse Huntingtin (Htt) expression in the CNS beginning during neural development, as well as reducing Htt expression only during embryonic and early postnatal stages, results in neurodegeneration in the adult brain. These findings suggest that HTT is important for the development and/or maintenance of the CNS, but they do not address the question of whether HTT is required specifically in the adult CNS for its normal functions and/or homeostasis. Recently, it was reported that although removing Htt expression in young adult mice causes lethality due to acute pancreatitis, loss of Htt expression in the adult brain is well tolerated and does not result in either motor deficits or neurodegeneration for up to 7 months after Htt inactivation. However, recent studies have also demonstrated that HTT participates in several cellular functions that are important for neuronal homeostasis and survival including sensing reactive oxygen species (ROS), DNA damage repair, and stress responses, in addition to its role in selective macroautophagy. In this review, HTT's functions in development and in the adult CNS will be discussed in the context of these recent discoveries, together with a discussion of their potential impact on the design of therapeutic strategies for Huntington's disease (HD) aimed at lowering total HTT expression.

Indexed as

AnimalsBrainHumansHuntingtin ProteinHuntington DiseaseHuntingtin Proteincell stressDNA damageHDHttHTTHuntingtinHuntington’s diseaseROS

Identifiers

PMID28339401
PMCPMC5389021
OpenAlexW2603868278

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.