Evidence map›Paper›PMID 28277568›Full record

ReviewMolecular neuropsychiatry2017

Neurodevelopmental Perspectives on Wnt Signaling in Psychiatry.

Kimberly A Mulligan, Benjamin N R Cheyette

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular neuropsychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
4.9field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 93 citations in OpenAlex.

  1. The involvement of the canonical Wnt-signaling receptor LRP5 and LRP6 gene variants with ADHD and sexual dimorphism: Association study and meta-analysis.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2019
    Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Excess Wnt in neurological disease.The Biochemical journal · 2025
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. ANKK1 Is a Wnt/PCP Scaffold Protein for Neural F-ACTIN Assembly.International journal of molecular sciences · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. NRF2, KEAP1 and GSK-3 levels in autism spectrum disorder: a case control study.International journal of developmental disabilities · 2024
    Article
  18. Molecular Landscape of Tourette's Disorder.International journal of molecular sciences · 2023
    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.

Kimberly A MulliganDepartment of Biological Sciences, California State University, Sacramento, CA, USA.
Benjamin N R CheyetteDepartment of Psychiatry, Kavli Institute for Fundamental Neuroscience, Weill Institute for Neurosciences, University of California San Francisco, San Francisco, CA, USA.
California State University, Sacramento · USUniversity of California, San Francisco · US

Funding

Neurobiological Mechanisms Underlying the Symptoms and Course of SchizophreniaT32MH089920 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI FORD, JUDITH M · 2010 to 2014
$1.3M
NIMH NIH HHS T32 MH089920
6 · The paper itself

Abstract

Mounting evidence indicates that Wnt signaling is relevant to pathophysiology of diverse mental illnesses including schizophrenia, bipolar disorder, and autism spectrum disorder. In the 35 years since Wnt ligands were first described, animal studies have richly explored how downstream Wnt signaling pathways affect an array of neurodevelopmental processes and how their disruption can lead to both neurological and behavioral phenotypes. Recently, human induced pluripotent stem cell (hiPSC) models have begun to contribute to this literature while pushing it in increasingly translational directions. Simultaneously, large-scale human genomic studies are providing evidence that sequence variation in Wnt signal pathway genes contributes to pathogenesis in several psychiatric disorders. This article reviews neurodevelopmental and postneurodevelopmental functions of Wnt signaling, highlighting mechanisms, whereby its disruption might contribute to psychiatric illness, and then reviews the most reliable recent genetic evidence supporting that mutations in Wnt pathway genes contribute to psychiatric illness. We are proponents of the notion that studies in animal and hiPSC models informed by the human genetic data combined with the deep knowledge base and tool kits generated over the last several decades of basic neurodevelopmental research will yield near-term tangible advances in neuropsychiatry.

Indexed as

Animal modelAutismBipolar disorderGenesGlycogen synthase kinase 3Induced pluripotent stem cellsLithiumMolecular psychiatryNeurodevelopmentSchizophreniaWnt signaling

Identifiers

PMID28277568
PMCPMC5318929
OpenAlexW2576097024

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.