Evidence map›Paper›PMID 28258509›Full record

ArticleNeuroscience bulletin2017

Distinct Defects in Spine Formation or Pruning in Two Gene Duplication Mouse Models of Autism.

Miao Wang, Huiping Li, Toru Takumi, Zilong Qiu, Xiu Xu, Xiang Yu, Wen-Jie Bian

Open access · hybridAbstract read
In one paragraph

Article in Neuroscience bulletin, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. mTOR-Dependent Spine Dynamics in Autism.Frontiers in molecular neuroscience · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Mathematical Models for Possible Roles of Oxytocin and Oxytocin Receptors in Autism.Computational and mathematical methods in medicine · 2019
    Article
  18. Frontiers in cellular neuroscience · 2019
    Article
  19. Article
  20. Review
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

7 authors at 4 institutions in 2 countries.

Miao WangInstitute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China.
Huiping LiDepartment of Child Healthcare, Children's Hospital of Fudan University, Shanghai, 201102, China.
Toru TakumiRIKEN Brain Science Institute, Wako, Saitama, 351-0198, Japan.
Zilong QiuInstitute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China.
Xiu XuDepartment of Child Healthcare, Children's Hospital of Fudan University, Shanghai, 201102, China. xuxiu@fudan.edu.cn.
Xiang YuInstitute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China. yuxiang@ion.ac.cn.
Wen-Jie BianInstitute of Neuroscience, State Key Laboratory of Neuroscience, CAS Center for Excellence in Brain Science and Intelligence Technology, Chinese Academy of Sciences, Shanghai, 200031, China. bwjflame@gmail.com.
University of Chinese Academy of Sciences · CNChildren's Hospital of Fudan University · CNChinese Academy of Sciences · CNRIKEN Center for Brain Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) encompasses a complex set of developmental neurological disorders, characterized by deficits in social communication and excessive repetitive behaviors. In recent years, ASD is increasingly being considered as a disease of the synapse. One main type of genetic aberration leading to ASD is gene duplication, and several mouse models have been generated mimicking these mutations. Here, we studied the effects of MECP2 duplication and human chromosome 15q11-13 duplication on synaptic development and neural circuit wiring in the mouse sensory cortices. We showed that mice carrying MECP2 duplication had specific defects in spine pruning, while the 15q11-13 duplication mouse model had impaired spine formation. Our results demonstrate that spine pathology varies significantly between autism models and that distinct aspects of neural circuit development may be targeted in different ASD mutations. Our results further underscore the importance of gene dosage in normal development and function of the brain.

Indexed as

Age FactorsAnalysis of VarianceAnimalsAutistic DisorderChromosomes, Human, Pair 15Dendritic SpinesDisease Models, AnimalGene DuplicationHumansMaleMethyl-CpG-Binding Protein 2MiceMice, Inbred C57BLMice, TransgenicSilver StainingSomatosensory CortexMECP2 protein, humanMethyl-CpG-Binding Protein 215q11-13 duplicationAutismAutism spectrum disorderGene duplicationMECP2SpineSpine formationSpine pruningSpinogenesis

Identifiers

PMID28258509
PMCPMC5360848
OpenAlexW2591876926

What OpenQuestion holds

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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.