Evidence map›Paper›PMID 30086265›Full record

ArticleBrain research2018

Neuronal subset-specific deletion of Pten results in aberrant Wnt signaling and memory impairments.

Samantha L Hodges, Conner D Reynolds, Gregory D Smith, Taylor S Jefferson, Nan Gao, Jessica B Morrison, Jessika White, Suzanne O Nolan, Joaquin N Lugo

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

Article in Brain research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. PTEN in Autism and Neurodevelopmental Disorders.Cold Spring Harbor perspectives in medicine · 2019
    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

9 authors at 4 institutions in 1 country.

Samantha L HodgesInstitute of Biomedical Studies, Baylor University, Waco, TX 76798, USA.
Conner D ReynoldsTexas College of Osteopathic Medicine, University of North Texas Health Science Center, Fort Worth, TX 76107, USA.
Gregory D SmithThe UCLA Brain Injury Research Center, Department of Neurosurgery, David Geffen School of Medicine at the University of California at Los Angeles, Los Angeles, CA 90095, USA.
Taylor S JeffersonDepartment of Psychology and Interdepartmental Neuroscience Program, Northwestern University, Evanston, IL 60208, USA.
Nan GaoDepartment of Psychology and Neuroscience, Baylor University, Waco, TX 76798, USA.
Jessica B MorrisonDepartment of Psychology and Neuroscience, Baylor University, Waco, TX 76798, USA.
Jessika WhiteDepartment of Psychology and Neuroscience, Baylor University, Waco, TX 76798, USA.
Suzanne O NolanDepartment of Psychology and Neuroscience, Baylor University, Waco, TX 76798, USA.
Joaquin N LugoInstitute of Biomedical Studies, Baylor University, Waco, TX 76798, USA; Department of Psychology and Neuroscience, Baylor University, Waco, TX 76798, USA; Department of Biology, Baylor University, Waco, TX 76798, USA. Electronic address: joaquin_lugo@baylor.edu.
Baylor University · USNorthwestern University · USUniversity of California, Los Angeles · USUniversity of North Texas Health Science Center · US

Funding

Signaling Mechanisms Underlying Epilepsy and Autism CormorbidityR15NS088776 · NINDS · BAYLOR UNIVERSITY · PI JOAQUIN N LUGO · 2015 to 2026
$1.8M
NINDS NIH HHS R15 NS088776
6 · The paper itself

Abstract

The canonical Wnt and PI3K/Akt/mTOR pathways both play critical roles in brain development early in life. There is extensive evidence of how each pathway is involved in neuronal and synaptic maturation, however, how these molecular networks interact requires further investigation. The present study examines the effect of neuronal subset-specific deletion of phosphatase and tensin homolog (Pten) in mice on Wnt signaling protein levels and associated cognitive impairments. PTEN functions as a negative regulator of the PI3K/Akt/mTOR pathway, and mutations in Pten can result in cognitive and behavioral impairments. We found that deletion of Pten resulted in elevated Dvl2, Wnt5a/b, and Naked2, along with decreased GSK3β hippocampal synaptosome protein expression compared to wild type mice. Aberrations in the canonical Wnt pathway were associated with learning and memory deficits in Pten knockout mice, specifically in novel object recognition and the Lashley maze. This study demonstrates that deletion of Pten not only significantly impacts PI3K/Akt/mTOR signaling, but affects proper functioning of the Wnt signaling pathway. Overall, these findings will help elucidate how the PI3K/Akt/mTOR pathway intersects with Wnt signaling to result in cognitive impairments, specifically in memory.

Indexed as

AnimalsBrainFemaleGene ExpressionLearning DisabilitiesMaleMemoryMemory DisordersMice, KnockoutNeuronsPTEN PhosphohydrolaseWnt Signaling PathwayPTEN PhosphohydrolasePten protein, mouseCanonicalLearningMemoryPI3K/Akt/mTORPtenWnt

Identifiers

PMID30086265
PMCPMC12994745
OpenAlexW2886637278

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.