Evidence map›Paper›PMID 27983565›Full record

ArticleJournal of Huntington's disease2016

LBH589, A Hydroxamic Acid-Derived HDAC Inhibitor, is Neuroprotective in Mouse Models of Huntington's Disease.

Vanita Chopra, Luisa Quinti, Prarthana Khanna, Paolo Paganetti, Rainer Kuhn, Anne B Young, Aleksey G Kazantsev, Steven Hersch

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of Huntington's disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

24 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Epigenetic regulation in Huntington's disease.Neurochemistry international · 2021
    Review
  16. New Avenues for the Treatment of Huntington's Disease.International journal of molecular sciences · 2021
    Review
  17. Article
  18. Article
  19. Review
  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

8 authors at 2 institutions in 2 countries.

Vanita ChopraDepartment of Neurology, Harvard Medical School, Massachusetts General Hospital, Charlestown, MA, USA.
Luisa QuintiDepartment of Neurology, Harvard Medical School, Massachusetts General Hospital, Charlestown, MA, USA.
Prarthana KhannaDepartment of Neurology, Harvard Medical School, Massachusetts General Hospital, Charlestown, MA, USA.
Paolo PaganettiNovartis Institutes for Biomedical Research, Basel, Switzerland.
Rainer KuhnNovartis Institutes for Biomedical Research, Basel, Switzerland.
Anne B YoungDepartment of Neurology, Harvard Medical School, Massachusetts General Hospital, Charlestown, MA, USA.
Aleksey G KazantsevDepartment of Neurology, Harvard Medical School, Massachusetts General Hospital, Charlestown, MA, USA.
Steven HerschDepartment of Neurology, Harvard Medical School, Massachusetts General Hospital, Charlestown, MA, USA.
Harvard University · USNovartis (Switzerland) · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundModulation of gene transcription by HDAC inhibitors has been shown repeatedly to be neuroprotective in cellular, invertebrate, and rodent models of Huntington's disease (HD). It has been difficult to translate these treatments to the clinic, however, because existing compounds have limited potency or brain bioavailability.

objectiveIn the present study, we assessed the therapeutic potential of LBH589, an orally bioavailable hydroxamic acid-derived nonselective HDAC inhibitor in mouse models of HD.

methodThe efficacy of LBH589 is tested in two HD mouse models using various biochemical, behavioral and neuropathological outcome measures.

resultsWe show that LBH589 crosses the blood brain barrier; induces histone hyperacetylation and prevents striatal neuronal shrinkage in R6/2 HD mice. In full-length knock-in HD mice LBH589-treatment improves motor performance and reduces neuronal atrophy.

conclusionsOur efficacious results of LBH589 in fragment and full-length mouse models of HD suggest that LBH589 is a promising candidate for clinical assessment in HD patients and provides confirmation that non-selective HDAC inhibitors can be viable clinical candidates.

Indexed as

AnimalsAtrophyCorpus StriatumDisease Models, AnimalFemaleGene Knock-In TechniquesHistone Deacetylase InhibitorsHistonesHuntington DiseaseHydroxamic AcidsIndolesMice, Inbred C57BLMice, Inbred CBAMice, TransgenicMotor ActivityNeuronsHistone Deacetylase InhibitorsHistonesHydroxamic AcidsIndolesNeuroprotective AgentsPanobinostatHDAC inhibitorhuntingtonneuroprotectionpanobinostat

Identifiers

PMID27983565
PMCPMC5181668
OpenAlexW2563191848

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.