Evidence map›Paper›PMID 26702437›Full record

ArticleScience advances2015

Structural-functional connectivity deficits of neocortical circuits in the Fmr1 (-/y) mouse model of autism.

Matthias G Haberl, Valerio Zerbi, Andor Veltien, Melanie Ginger, Arend Heerschap, Andreas Frick

Abstract read
In one paragraph

Article in Science advances, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

57 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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  6. Biological subtyping of autism via cross-species fMRI.bioRxiv : the preprint server for biology · 2025
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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

6 authors.

Matthias G HaberlINSERM, Neurocentre Magendie, Physiopathologie de la plasticité neuronale, U862, 33077 Bordeaux, France. ; University of Bordeaux, Neurocentre Magendie, Physiopathologie de la plasticité neuronale, U862, 33076 Bordeaux, France. ; Institute of NeuroInformatics, University of Zurich, 8057 Zurich, Switzerland.ORCID 0000-0002-4961-7832
Valerio ZerbiBiomedical MR Research Group, Department of Radiology and Nuclear Medicine, Radboud University Medical Center, 6500 Nijmegen, Netherlands.
Andor VeltienBiomedical MR Research Group, Department of Radiology and Nuclear Medicine, Radboud University Medical Center, 6500 Nijmegen, Netherlands.
Melanie GingerINSERM, Neurocentre Magendie, Physiopathologie de la plasticité neuronale, U862, 33077 Bordeaux, France. ; University of Bordeaux, Neurocentre Magendie, Physiopathologie de la plasticité neuronale, U862, 33076 Bordeaux, France.
Arend HeerschapBiomedical MR Research Group, Department of Radiology and Nuclear Medicine, Radboud University Medical Center, 6500 Nijmegen, Netherlands.ORCID 0000-0001-9930-4562
Andreas FrickINSERM, Neurocentre Magendie, Physiopathologie de la plasticité neuronale, U862, 33077 Bordeaux, France. ; University of Bordeaux, Neurocentre Magendie, Physiopathologie de la plasticité neuronale, U862, 33076 Bordeaux, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fragile X syndrome (FXS), the most common inherited form of intellectual disability disorder and a frequent cause of autism spectrum disorder (ASD), is characterized by a high prevalence of sensory symptoms. Perturbations in the anatomical connectivity of neocortical circuits resulting in their functional defects have been hypothesized to contribute to the underlying etiology of these disorders. We tested this idea by probing alterations in the functional and structural connectivity of both local and long-ranging neocortical circuits in the Fmr1 (-/y) mouse model of FXS. To achieve this, we combined in vivo ultrahigh-field diffusion tensor magnetic resonance imaging (MRI), functional MRI, and viral tracing approaches in adult mice. Our results show an anatomical hyperconnectivity phenotype for the primary visual cortex (V1), but a disproportional low connectivity of V1 with other neocortical regions. These structural data are supported by defects in the structural integrity of the subcortical white matter in the anterior and posterior forebrain. These anatomical alterations might contribute to the observed functional decoupling across neocortical regions. We therefore identify FXS as a "connectopathy," providing a translational model for understanding sensory processing defects and functional decoupling of neocortical areas in FXS and ASD.

Indexed as

AutismbiomarkerconnectopathyDTIfMRIFragile X Syndromefunctional connectivityneocortexretrograde tracingstructural connectivity

Identifiers

PMID26702437
PMCPMC4681325

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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.