Evidence map›Paper›PMID 21364941›Full record

ArticlePloS one2011

Genetic-background modulation of core and variable autistic-like symptoms in Fmr1 knock-out mice.

Susanna Pietropaolo, Aurélie Guilleminot, Benoît Martin, Francesca R D'Amato, Wim E Crusio

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
8.4field-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

89 citing papers in PubMed, 174 citations in OpenAlex.

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  12. Mapping the landscape of social behavior.bioRxiv : the preprint server for biology · 2024
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  20. Hyperacusis in the AdultInternational journal of molecular sciences · 2023
    Article

29 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

5 authors at 3 institutions in 2 countries.

Susanna PietropaoloInstitut de Neurosciences Cognitives et Intégratives d'Aquitaine, Université de Bordeaux and CNRS UMR 5287, Talence, France.
Aurélie Guilleminot
Benoît Martin
Francesca R D'Amato
Wim E Crusio
Centre National de la Recherche Scientifique · FRInserm · FRNational Academies of Sciences, Engineering, and Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNo animal models of autism spectrum disorders (ASD) with good construct validity are currently available; using genetic models of pathologies characterized by ASD-like deficits, but with known causes, may be therefore a promising strategy. The Fmr1-KO mouse is an example of this approach, modeling Fragile X syndrome, a well-known genetic disorder presenting ASD symptoms. The Fmr1-KO is available on different genetic backgrounds (FVB versus C57BL/6), which may explain some of the conflicting results that have been obtained with these mutants up till now.

methodsFmr1 KO and their wild-type littermates on both the FVB and C57BL/6 genetic backgrounds were examined on a battery of tests modeling the clinical symptoms of ASD, including the triad of core symptoms (alterations in social interaction and communication, presence of repetitive behaviors), as well as the secondary symptoms (disturbances in sensori-motor reactivity and in circadian patterns of activity, epileptic events).

resultsFmr1-KO mice displayed autistic-like core symptoms of altered social interaction and occurrence of repetitive behaviors with additional hyperactivity. The genetic background modulated the effects of the Fmr1 deletion and it appears that the C57BL/6 background may be more suitable for further research on core autistic-like symptoms.

conclusionsThe Fmr1-mouse line does not recapitulate all of the main core and secondary ASD symptoms, but still can be useful to elucidate the neurobiological mechanisms underlying specific ASD-like endophenotypes.

Indexed as

AnimalsAutistic DisorderBehavior, AnimalDisease Models, AnimalEndophenotypesFragile X Messenger Ribonucleoprotein 1Genetic HeterogeneityGenetic Predisposition to DiseaseLearningMaleMiceMice, Inbred C57BLMice, KnockoutMotor ActivityPhenotypeFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1

Identifiers

PMID21364941
PMCPMC3043074
OpenAlexW2002465714

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.