Evidence map›Paper›PMID 38267530›Full record

ArticleScientific reports2024

Dose-dependent reduction of somatic expansions but not Htt aggregates by di-valent siRNA-mediated silencing of MSH3 in HdhQ111 mice.

Rachelle Driscoll, Lucas Hampton, Neeta A Abraham, J Douglas Larigan, Nadine F Joseph, Juan C Hernandez-Vega, Sarah Geisler, Fu-Chia Yang, Matthew Deninger, David T Tran and 10 more

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

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Huntington's Disease: Complex Pathogenesis and Therapeutic Strategies.International journal of molecular sciences · 2024
    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

20 authors at 1 institution in 1 country.

Rachelle Driscoll *Translational Sciences, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Lucas Hampton *Neurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Neeta A Abraham *Neurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
J Douglas LariganBiotherapeutics and Medicinal Sciences, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Nadine F JosephNeurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Juan C Hernandez-VegaNeurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Sarah GeislerTranslational Sciences, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Fu-Chia YangTranslational Sciences, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Matthew DeningerAtalanta Therapeutics, 51 Sleeper Street, Boston, MA, 02210, USA.
David T TranAtalanta Therapeutics, 51 Sleeper Street, Boston, MA, 02210, USA.
Natasha KhatriAtalanta Therapeutics, 51 Sleeper Street, Boston, MA, 02210, USA.
Bruno M D C GodinhoAtalanta Therapeutics, 51 Sleeper Street, Boston, MA, 02210, USA.
Garth A KinbergerAtalanta Therapeutics, 51 Sleeper Street, Boston, MA, 02210, USA.
Daniel R MontagnaNeurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Warren D HirstNeurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Catherine L GuardadoNeurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Kelly E GlajchNeurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
H Moore ArnoldTranslational Sciences, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA.
Corrie L Gallant-BehmAtalanta Therapeutics, 51 Sleeper Street, Boston, MA, 02210, USA.
Andreas WeihofenNeurodegenerative Diseases Research Unit, Biogen, 225 Binney Street, Cambridge, MA, 02142, USA. andreas.weihofen@biogen.com.
Biogen (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is a progressive neurodegenerative disorder caused by CAG trinucleotide repeat expansions in exon 1 of the HTT gene. In addition to germline CAG expansions, somatic repeat expansions in neurons also contribute to HD pathogenesis. The DNA mismatch repair gene, MSH3, identified as a genetic modifier of HD onset and progression, promotes somatic CAG expansions, and thus presents a potential therapeutic target. However, what extent of MSH3 protein reduction is needed to attenuate somatic CAG expansions and elicit therapeutic benefits in HD disease models is less clear. In our study, we employed potent di-siRNAs to silence mouse Msh3 mRNA expression in a dose-dependent manner in Hdh

Indexed as

Corpus StriatumHuntington DiseaseAnimalsExonsHuntingtin ProteinMiceMutS Homolog 3 ProteinRNA InterferenceRNA, MessengerRNA, Small InterferingHtt protein, mouseHuntingtin ProteinMsh3 protein, mouseMutS Homolog 3 ProteinRNA, MessengerRNA, Small Interfering

Identifiers

PMID38267530
PMCPMC10808119
OpenAlexW4391168869

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.