Evidence map›Paper›PMID 18625318›Full record

ArticleMolecular and cellular neurosciences2009

Expanded CAG repeats in the murine Huntington's disease gene increases neuronal differentiation of embryonic and neural stem cells.

Matthew T Lorincz, Virginia A Zawistowski

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular neurosciences, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.8field-weighted citation impact, top 33% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

  1. Exploring huntington's disease from a neurodevelopmental perspective.International journal of biological sciences · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. From Progenitors to Progeny: Shaping Striatal Circuit Development and Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  7. Review
  8. Article
  9. Article
  10. Selective expression of mutant huntingtin during development recapitulates characteristic features of Huntington's disease.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  11. Review
  12. Article
  13. Modeling Huntington's disease with induced pluripotent stem cells.Molecular and cellular neurosciences · 2013
    Review
  14. Extensive changes in DNA methylation are associated with expression of mutant huntingtin.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  15. Article
  16. Article
  17. Article
  18. Multiple phenotypes in Huntington disease mouse neural stem cells.Molecular and cellular neurosciences · 2012
    Article
  19. Article
  20. 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 2 institutions in 1 country.

Matthew T LorinczDepartment of Neurology, University of Michigan School of Medicine, 1500 E. Medical Center Drive, Ann Arbor, MI 48109-2200, USA. lorincz@umich.edu
Virginia A Zawistowski
Michigan Medicine · USUniversity of Michigan–Ann Arbor · US

Funding

Embryonic Stem Cell Model of Polyglutamine DiseaseK08NS045180 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LORINCZ, MATTHEW T · 2003 to 2007
$852k
NINDS NIH HHS K08 NS045180NINDS NIH HHS NS45180
6 · The paper itself

Abstract

Huntington's disease is an uncommon autosomal dominant neurodegenerative disorder caused by expanded polyglutamine repeats. Increased neurogenesis was demonstrated recently in Huntington's disease post-mortem samples. In this manuscript, neuronally differentiated embryonic stem cells with expanded CAG repeats in the murine Huntington's disease homologue and neural progenitors isolated from the subventricular zone of an accurate mouse Huntington's disease were examined for increased neurogenesis. Embryonic stem cells with expanded CAG repeats in the murine Huntington's disease homologue were demonstrated to undergo facilitated differentiation first into neural progenitors, then into more mature neurons. Neural progenitor cells isolated from the subventricular zone of a Huntington's disease knock-in animal displayed increased production of neural progenitors and increased neurogenesis. These findings suggested that neuronally differentiating embryonic stem cells with expanded CAG repeats is a reasonable system to identify factors responsible for increased neurogenesis in Huntington's disease. Expression profiling analysis comparing neuronally differentiating embryonic stem cells with expanded CAG repeats to neuronally differentiating embryonic stem cells without expanded CAG repeats identified transcripts involved in development and transcriptional regulation as factors possibly mediating increased neurogenesis in response to expanded CAG repeats.

Indexed as

Trinucleotide Repeat ExpansionAnimalsBiomarkersCell CycleCell DeathCell DifferentiationCell LineageDisease Models, AnimalEmbryonic Stem CellsGene Expression ProfilingHumansHuntingtin ProteinHuntington DiseaseMiceNerve Tissue ProteinsNeurogenesisBiomarkersHtt protein, mouseHuntingtin ProteinNerve Tissue ProteinsNuclear Proteins

Identifiers

PMID18625318
PMCPMC2666278
OpenAlexW2070557152

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.