Evidence map›Paper›PMID 17848915›Full record

ReviewMolecular psychiatry2008

Advances in behavioral genetics: mouse models of autism.

S S Moy, J J Nadler

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular psychiatry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
6.3field-weighted citation impact, top 3% 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

104 citing papers in PubMed, 216 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
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  6. Impaired AIS plasticity in ankyrin-G mutant mice alters cortical excitability and behavior.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  8. Review
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  16. Review
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  20. Review

44 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

2 authors at 1 institution in 1 country.

S S MoyNeurodevelopmental Disorders Research Center, Department of Psychiatry, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, USA. ssmoy@med.unc.edu
J J Nadler
University of North Carolina at Chapel Hill · US

Funding

UNC MRDD Research CenterP30HD003110 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BELGER, AYSENIL · 1985 to 2012
$28.7M
TREATMENT PROJECTU54MH066418 · NIMH · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PIVEN, JOSEPH · 2002 to 2006
$7.9M
NICHD NIH HHS P30 HD03110NIMH NIH HHS U54 MH66418
6 · The paper itself

Abstract

Autism is a neurodevelopmental syndrome with markedly high heritability. The diagnostic indicators of autism are core behavioral symptoms, rather than definitive neuropathological markers. Etiology is thought to involve complex, multigenic interactions and possible environmental contributions. In this review, we focus on genetic pathways with multiple members represented in autism candidate gene lists. Many of these pathways can also be impinged upon by environmental risk factors associated with the disorder. The mouse model system provides a method to experimentally manipulate candidate genes for autism susceptibility, and to use environmental challenges to drive aberrant gene expression and cell pathology early in development. Mouse models for fragile X syndrome, Rett syndrome and other disorders associated with autistic-like behavior have elucidated neuropathology that might underlie the autism phenotype, including abnormalities in synaptic plasticity. Mouse models have also been used to investigate the effects of alterations in signaling pathways on neuronal migration, neurotransmission and brain anatomy, relevant to findings in autistic populations. Advances have included the evaluation of mouse models with behavioral assays designed to reflect disease symptoms, including impaired social interaction, communication deficits and repetitive behaviors, and the symptom onset during the neonatal period. Research focusing on the effect of gene-by-gene interactions or genetic susceptibility to detrimental environmental challenges may further understanding of the complex etiology for autism.

Indexed as

Disease Models, AnimalGenetic Predisposition to DiseaseAnimalsAutistic DisorderFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeGenetics, BehavioralMethyl-CpG-Binding Protein 2MiceMice, Mutant StrainsPhenotypeRett SyndromeSynapsesFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1Methyl-CpG-Binding Protein 2

Identifiers

PMID17848915
OpenAlexW2099464916

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.