Evidence map›Paper›PMID 27133257›Full record

ReviewBiomolecules & therapeutics2016

Clinical and Neurobiological Relevance of Current Animal Models of Autism Spectrum Disorders.

Ki Chan Kim, Edson Luck Gonzales, María T Lázaro, Chang Soon Choi, Geon Ho Bahn, Hee Jeong Yoo, Chan Young Shin

Open access · greenAbstract readReview
In one paragraph

Review in Biomolecules & therapeutics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  4. Article
  5. Review
  6. Article
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  9. Article
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  11. Article
  12. Article
  13. Opposite Expression Patterns ofFrontiers in psychiatry · 2019
    Article
  14. Article
  15. Article
  16. Article
  17. Evidence for Brainstem Contributions to Autism Spectrum Disorders.Frontiers in integrative neuroscience · 2018
    Review
  18. 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 5 institutions in 2 countries.

Ki Chan KimDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
Edson Luck GonzalesCenter for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, Konkuk University, Seoul 05029, Republic of Korea.
María T LázaroProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Chang Soon ChoiCenter for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, Konkuk University, Seoul 05029, Republic of Korea.
Geon Ho BahnDepartment of Neuropsychiatry, School of Medicine, Kyung Hee University, Seoul 02447, Republic of Korea.
Hee Jeong YooDepartment of Neuropsychiatry, Seoul National University Bungdang Hospital, Seongnam 13620, Republic of Korea.
Chan Young ShinCenter for Neuroscience Research, SMART Institute of Advanced Biomedical Sciences, Konkuk University, Seoul 05029, Republic of Korea.
Konkuk University · KRKyung Hee University · KRSeoul National University Bundang Hospital · KRThe University of Texas Southwestern Medical Center · USUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by social and communication impairments, as well as repetitive and restrictive behaviors. The phenotypic heterogeneity of ASD has made it overwhelmingly difficult to determine the exact etiology and pathophysiology underlying the core symptoms, which are often accompanied by comorbidities such as hyperactivity, seizures, and sensorimotor abnormalities. To our benefit, the advent of animal models has allowed us to assess and test diverse risk factors of ASD, both genetic and environmental, and measure their contribution to the manifestation of autistic symptoms. At a broader scale, rodent models have helped consolidate molecular pathways and unify the neurophysiological mechanisms underlying each one of the various etiologies. This approach will potentially enable the stratification of ASD into clinical, molecular, and neurophenotypic subgroups, further proving their translational utility. It is henceforth paramount to establish a common ground of mechanistic theories from complementing results in preclinical research. In this review, we cluster the ASD animal models into lesion and genetic models and further classify them based on the corresponding environmental, epigenetic and genetic factors. Finally, we summarize the symptoms and neuropathological highlights for each model and make critical comparisons that elucidate their clinical and neurobiological relevance.

Indexed as

Animal modelsAutism spectrum disordersClinical relevanceEnvironmental factorsGenetic factors

Identifiers

PMID27133257
PMCPMC4859786
OpenAlexW2345066662

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.