Evidence map›Paper›PMID 26881141›Full record

ReviewNeural plasticity2016

Synaptic Wnt/GSK3β Signaling Hub in Autism.

Mario O Caracci, Miguel E Ávila, Giancarlo V De Ferrari

Open access · goldAbstract readReview
In one paragraph

Review in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 2 pooled it
9.0field-weighted citation impact, top 2% 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

45 citing papers in PubMed, 2 syntheses or guidelines pooled it, 71 citations in OpenAlex.

  1. Pooled it
  2. 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
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. NRF2, KEAP1 and GSK-3 levels in autism spectrum disorder: a case control study.International journal of developmental disabilities · 2024
    Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Wdfy3 regulates glycophagy, mitophagy, and synaptic plasticity.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Mario O CaracciCenter for Biomedical Research, Faculty of Biological Sciences and Faculty of Medicine, Universidad Andres Bello, P.O. Box 8370134, Santiago, Chile; FONDAP Center for Genome Regulation, Santiago, Chile.
Miguel E ÁvilaCenter for Biomedical Research, Faculty of Biological Sciences and Faculty of Medicine, Universidad Andres Bello, P.O. Box 8370134, Santiago, Chile; FONDAP Center for Genome Regulation, Santiago, Chile.
Giancarlo V De FerrariCenter for Biomedical Research, Faculty of Biological Sciences and Faculty of Medicine, Universidad Andres Bello, P.O. Box 8370134, Santiago, Chile; FONDAP Center for Genome Regulation, Santiago, Chile.
Universidad Andrés Bello · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hundreds of genes have been associated with autism spectrum disorders (ASDs) and the interaction of weak and de novo variants derive from distinct autistic phenotypes thus making up the "spectrum." The convergence of these variants in networks of genes associated with synaptic function warrants the study of cell signaling pathways involved in the regulation of the synapse. The Wnt/β-catenin signaling pathway plays a central role in the development and regulation of the central nervous system and several genes belonging to the cascade have been genetically associated with ASDs. In the present paper, we review basic information regarding the role of Wnt/β-catenin signaling in excitatory/inhibitory balance (E/I balance) through the regulation of pre- and postsynaptic compartments. Furthermore, we integrate information supporting the role of the glycogen synthase kinase 3β (GSK3β) in the onset/development of ASDs through direct modulation of Wnt/β-catenin signaling. Finally, given GSK3β activity as key modulator of synaptic plasticity, we explore the potential of this kinase as a therapeutic target for ASD.

Indexed as

Wnt Signaling PathwayAnimalsAutism Spectrum DisorderBrainGlycogen Synthase Kinase 3 betaHumansSynapsesGlycogen Synthase Kinase 3 beta

Identifiers

PMID26881141
PMCPMC4736967
OpenAlexW2222900840

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.