Evidence map›Paper›PMID 27909399›Full record

ReviewFrontiers in cellular neuroscience2016

A Subset of Autism-Associated Genes Regulate the Structural Stability of Neurons.

Yu-Chih Lin, Jeannine A Frei, Michaela B C Kilander, Wenjuan Shen, Gene J Blatt

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing 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

62 citing papers in PubMed, 101 citations in OpenAlex.

  1. Article
  2. Maternal Extracellular Vesicles During Pregnancy and Autism Risk in Children.medRxiv : the preprint server for health sciences · 2026
    Article
  3. bioRxiv : the preprint server for biology · 2026
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  17. FMRP Enhances the Translation ofInternational journal of molecular sciences · 2023
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  20. Article

2 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 1 institution in 1 country.

Yu-Chih LinLaboratory of Neuronal Connectivity, Program in Neuroscience, Hussman Institute for Autism, Baltimore MD, USA.
Jeannine A FreiLaboratory of Neuronal Connectivity, Program in Neuroscience, Hussman Institute for Autism, Baltimore MD, USA.
Michaela B C KilanderLaboratory of Neuronal Connectivity, Program in Neuroscience, Hussman Institute for Autism, Baltimore MD, USA.
Wenjuan ShenLaboratory of Neuronal Connectivity, Program in Neuroscience, Hussman Institute for Autism, Baltimore MD, USA.
Gene J BlattLaboratory of Autism Neurocircuitry, Program in Neuroscience, Hussman Institute for Autism, Baltimore MD, USA.
Hussman Institute for Autism · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autism spectrum disorder (ASD) comprises a range of neurological conditions that affect individuals' ability to communicate and interact with others. People with ASD often exhibit marked qualitative difficulties in social interaction, communication, and behavior. Alterations in neurite arborization and dendritic spine morphology, including size, shape, and number, are hallmarks of almost all neurological conditions, including ASD. As experimental evidence emerges in recent years, it becomes clear that although there is broad heterogeneity of identified autism risk genes, many of them converge into similar cellular pathways, including those regulating neurite outgrowth, synapse formation and spine stability, and synaptic plasticity. These mechanisms together regulate the structural stability of neurons and are vulnerable targets in ASD. In this review, we discuss the current understanding of those autism risk genes that affect the structural connectivity of neurons. We sub-categorize them into (1) cytoskeletal regulators, e.g., motors and small RhoGTPase regulators; (2) adhesion molecules, e.g., cadherins, NCAM, and neurexin superfamily; (3) cell surface receptors, e.g., glutamatergic receptors and receptor tyrosine kinases; (4) signaling molecules, e.g., protein kinases and phosphatases; and (5) synaptic proteins, e.g., vesicle and scaffolding proteins. Although the roles of some of these genes in maintaining neuronal structural stability are well studied, how mutations contribute to the autism phenotype is still largely unknown. Investigating whether and how the neuronal structure and function are affected when these genes are mutated will provide insights toward developing effective interventions aimed at improving the lives of people with autism and their families.

Indexed as

actinadhesion moleculeautism-risk genesdendritedendritic spineneurite outgrowthsynapse formation

Identifiers

PMID27909399
PMCPMC5112273
OpenAlexW2550096096

What OpenQuestion holds

Textmetadata
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.