Evidence map›Paper›PMID 27651147›Full record

ArticleNeuroscience2016

Memory deficits, gait ataxia and neuronal loss in the hippocampus and cerebellum in mice that are heterozygous for Pur-alpha.

Mary F Barbe, Jessica J Krueger, Regina Loomis, Jessica Otte, Jennifer Gordon

Abstract read
In one paragraph

Article in Neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
1.0field-weighted citation impact, top 21% 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, 2 syntheses or guidelines pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Heterozygous c.175C>T variant inClinical case reports · 2023
    Article
  11. Article
  12. Review
  13. Article
  14. Role of circRNA in pathogenesis of AlzheimerZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022
    Article
  15. Article
  16. Neurology. Genetics · 2021
    Article
  17. Complex Movement Disorders in a Boy with PURA Syndrome.Movement disorders clinical practice · 2021
    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

5 authors at 1 institution in 1 country.

Mary F BarbeDepartment of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, PA, USA; Comprehensive NeuroAIDS Center, Temple University School of Medicine, Philadelphia, PA, USA. Electronic address: mary.barbe@temple.edu.
Jessica J KruegerComprehensive NeuroAIDS Center, Temple University School of Medicine, Philadelphia, PA, USA.
Regina LoomisComprehensive NeuroAIDS Center, Temple University School of Medicine, Philadelphia, PA, USA.
Jessica OtteDepartment of Neuroscience and Center for Neurovirology, Temple University School of Medicine, Philadelphia, PA, USA; Comprehensive NeuroAIDS Center, Temple University School of Medicine, Philadelphia, PA, USA.
Jennifer GordonDepartment of Neuroscience and Center for Neurovirology, Temple University School of Medicine, Philadelphia, PA, USA; Comprehensive NeuroAIDS Center, Temple University School of Medicine, Philadelphia, PA, USA.
Temple University · US

Funding

Viral Gene Editing and Bioinformatics Core for Institution # 269291P30MH092177 · NIMH · TEMPLE UNIV OF THE COMMONWEALTH · PI Ilker Kudret Sariyer · 2011 to 2026
$24.9M
NIMH NIH HHS P30 MH092177
6 · The paper itself

Abstract

Pur-alpha is a highly conserved sequence-specific DNA and RNA binding protein with established roles in DNA replication, RNA translation, cell cycle regulation, and maintenance of neuronal differentiation. Prior studies have shown that mice lacking Pur-alpha (-/-) display decreased neurogenesis and impaired neuronal differentiation. We sought to examine for the first time, the behavioral phenotype and brain histopathology of mice that are heterozygous (+/-) for Pur-alpha. Standardized behavioral phenotyping revealed a decreased escape response to touch, limb and abdominal hypotonia, and gait abnormalities in heterozygous Pur-alpha (+/-) mice, compared to wild-type (+/+) littermates. Footprint pattern analyses showed wider-based steps, increased missteps and more outwardly rotated hindpaws in heterozygous Pur-alpha (+/-) mice, suggestive of cerebellar pathology. The Barnes maze and novel object location testing revealed significant memory deficits in heterozygous Pur-alpha mice, suggestive of hippocampal pathology. Quantitative immunohistochemical assays of the vermal region of the cerebellum and CA1-3 regions of the hippocampus revealed reduced numbers of neurons in general, as well as reduced numbers of Pur-alpha+-immunopositive neurons and dendrites in heterozygous Pur-alpha mice, compared to wild-type littermates. Past studies have implicated mutations in Pur-alpha in several diseases of brain development and neurodegeneration. When combined with these new findings, the Pur-alpha heterozygous knockout mice may provide an animal model to study mechanisms of and treatments for Pur-alpha-related cognitive deficiencies and neuropathology.

Indexed as

AnimalsBehavior, AnimalBrainCerebellumDNA-Binding ProteinsGait AtaxiaHeterozygoteHippocampusMemory DisordersMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeuronsDNA-Binding ProteinsNerve Tissue ProteinsPura protein, mouseanimalsbrain pathologyknockoutmicePURApuralpha

Identifiers

PMID27651147
PMCPMC5458736
OpenAlexW2519114378

What OpenQuestion holds

Textmetadata
LicenceTDM
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.