Evidence map›Paper›PMID 26403076›Full record

ReviewGenes, brain, and behavior2016

Behavioral phenotypes of genetic mouse models of autism.

T M Kazdoba, P T Leach, J N Crawley

Open access · bronzeAbstract readReview
In one paragraph

Review in Genes, brain, and behavior, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed
7.6field-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

102 citing papers in PubMed, 186 citations in OpenAlex.

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  18. Prosodic Differences in Women with theInternational journal of molecular sciences · 2025
    Article
  19. Behavioral Physiology of the CNTNAP2 Knockout Mouse.HSOA trends in anatomy and physiology · 2025
    Article
  20. Article

42 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.

T M KazdobaMIND Institute, Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, CA, USA.
P T LeachMIND Institute, Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, CA, USA.
J N CrawleyMIND Institute, Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, CA, USA.
University of California, Davis · US

Funding

Rodent Behavior CoreU54HD079125 · NICHD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI ABBEDUTO, LEONARD J. · 2013 to 2019
$8.5M
Interdisciplinary Training for Autism Researchers(RMI)T32MH073124 · NIMH · UNIVERSITY OF CALIFORNIA DAVIS · PI Stephen Charles Noctor, Christine Wu Nordahl · 2004 to 2026
$6.8M
Convergent Synaptic Mechanisms in Neurodevelopmental DisordersR01NS085709 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CRAWLEY, JACQUELINE N, GALL, CHRISTINE M · 2013 to 2017
$2.8M
NICHD NIH HHS U54 HD079125NIMH NIH HHS MH0073124NIMH NIH HHS T32 MH073124NINDS NIH HHS 1R01NS085709-01NINDS NIH HHS R01 NS085709
6 · The paper itself

Abstract

More than a hundred de novo single gene mutations and copy-number variants have been implicated in autism, each occurring in a small subset of cases. Mutant mouse models with syntenic mutations offer research tools to gain an understanding of the role of each gene in modulating biological and behavioral phenotypes relevant to autism. Knockout, knockin and transgenic mice incorporating risk gene mutations detected in autism spectrum disorder and comorbid neurodevelopmental disorders are now widely available. At present, autism spectrum disorder is diagnosed solely by behavioral criteria. We developed a constellation of mouse behavioral assays designed to maximize face validity to the types of social deficits and repetitive behaviors that are central to an autism diagnosis. Mouse behavioral assays for associated symptoms of autism, which include cognitive inflexibility, anxiety, hyperactivity, and unusual reactivity to sensory stimuli, are frequently included in the phenotypic analyses. Over the past 10 years, we and many other laboratories around the world have employed these and additional behavioral tests to phenotype a large number of mutant mouse models of autism. In this review, we highlight mouse models with mutations in genes that have been identified as risk genes for autism, which work through synaptic mechanisms and through the mTOR signaling pathway. Robust, replicated autism-relevant behavioral outcomes in a genetic mouse model lend credence to a causal role for specific gene contributions and downstream biological mechanisms in the etiology of autism.

Indexed as

Behavior, AnimalDisease Models, AnimalGenetic Predisposition to DiseasePhenotypeAnimalsAutistic DisorderHumansMiceTOR Serine-Threonine KinasesTOR Serine-Threonine KinasesAnxiety-likeautismcognitiongeneshyperactivitymicemutant modelsneurodevelopmentalrepetitive behaviorsensory reactivitysociabilitysocial behaviorvocalizations

Identifiers

PMID26403076
PMCPMC4775274
OpenAlexW2120312409

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.