Evidence map›Paper›PMID 24605088›Full record

ReviewFrontiers in cellular neuroscience2014

Genetic aspects of autism spectrum disorders: insights from animal models.

Swati Banerjee, Maeveen Riordan, Manzoor A Bhat

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
9.9field-weighted citation impact, top 1% 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

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 136 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Review
  5. Review
  6. Review
  7. From Genetics to Function: the Role of ABCA12 in Autism Neurobiology.Journal of molecular neuroscience : MN · 2025
    Review
  8. Article
  9. Oxytocin treatment rescues irritability-like behavior in Cc2d1a conditional knockout mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  10. Decoding the genetic landscape of autism: A comprehensive review.World journal of clinical pediatrics · 2024
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. The Roles of Par3, Par6, and aPKC Polarity Proteins in Normal Neurodevelopment and in Neurodegenerative and Neuropsychiatric Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Review
  17. Article
  18. Article
  19. Review
  20. Review

6 more citing papers are in PubMed but not listed here.

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.

Swati BanerjeeDepartment of Physiology, Center for Biomedical Neuroscience, School of Medicine, University of Texas Health Science Center San Antonio, TX, USA.
Maeveen RiordanDepartment of Physiology, Center for Biomedical Neuroscience, School of Medicine, University of Texas Health Science Center San Antonio, TX, USA.
Manzoor A BhatDepartment of Physiology, Center for Biomedical Neuroscience, School of Medicine, University of Texas Health Science Center San Antonio, TX, USA.
The University of Texas Health Science Center at San Antonio · US

Funding

Molecular Organization &Function of Paranodal JunctionsR01GM063074 · NIGMS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BHAT, MANZOOR A. · 2001 to 2023
$5.8M
Molecular Characterization of Axon-Glial InteractionsR01NS050356 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BHAT, MANZOOR A. · 2006 to 2016
$2.9M
NIGMS NIH HHS R01 GM063074NINDS NIH HHS R01 NS050356
6 · The paper itself

Abstract

Autism spectrum disorders (ASDs) are a complex neurodevelopmental disorder that display a triad of core behavioral deficits including restricted interests, often accompanied by repetitive behavior, deficits in language and communication, and an inability to engage in reciprocal social interactions. ASD is among the most heritable disorders but is not a simple disorder with a singular pathology and has a rather complex etiology. It is interesting to note that perturbations in synaptic growth, development, and stability underlie a variety of neuropsychiatric disorders, including ASD, schizophrenia, epilepsy, and intellectual disability. Biological characterization of an increasing repertoire of synaptic mutants in various model organisms indicates synaptic dysfunction as causal in the pathophysiology of ASD. Our understanding of the genes and genetic pathways that contribute toward the formation, stabilization, and maintenance of functional synapses coupled with an in-depth phenotypic analysis of the cellular and behavioral characteristics is therefore essential to unraveling the pathogenesis of these disorders. In this review, we discuss the genetic aspects of ASD emphasizing on the well conserved set of genes and genetic pathways implicated in this disorder, many of which contribute to synapse assembly and maintenance across species. We also review how fundamental research using animal models is providing key insights into the various facets of human ASD.

Indexed as

animal modelsautism spectrum disordercell adhesion moleculesenvironmentepigeneticsgeneticsscaffolding proteinssynapse

Identifiers

PMID24605088
PMCPMC3932417
OpenAlexW2064683298

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.