Dendritic spine and synapse pathology in chromatin modifier-associated autism spectrum disorders and intellectual disability

Formation of dendritic spine and synapse is an essential final step of brain wiring to establish functional communication in the developing brain. Recent findings have displayed altered dendritic spine and synapse morphogenesis, plasticity, and related molecular mechanisms in animal models and post-...

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Published inFrontiers in molecular neuroscience Vol. 15; p. 1048713
Main Authors Ford, Thomas James L., Jeon, Byeong Tak, Lee, Hyunkyoung, Kim, Woo-Yang
Format Journal Article
LanguageEnglish
Published Switzerland Frontiers Research Foundation 19.01.2023
Frontiers Media S.A
Subjects
Animal models
ARID1B
Autism
Behavior
Brain research
Chromatin remodeling
Dendritic plasticity
dendritic spine
Dendritic spines
Gene expression
Intellectual disabilities
KANSL1
Molecular modelling
Morphogenesis
Morphology
Mutation
Neurodevelopmental disorders
Neuroscience
Proteins
Susceptibility
synapse
WDR5
KANSL1
WDR5
dendritic spine
synapse
ARID1B
autism
intellectual disability
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Summary:Formation of dendritic spine and synapse is an essential final step of brain wiring to establish functional communication in the developing brain. Recent findings have displayed altered dendritic spine and synapse morphogenesis, plasticity, and related molecular mechanisms in animal models and post-mortem human brains of autism spectrum disorders (ASD) and intellectual disability (ID). Many genes and proteins are shown to be associated with spines and synapse development, and therefore neurodevelopmental disorders. In this review, however, particular attention will be given to chromatin modifiers such as AT-Rich Interactive Domain 1B (ARID1B), KAT8 regulatory non-specific lethal (NSL) complex subunit 1 (KANSL1), and WD Repeat Domain 5 (WDR5) which are among strong susceptibility factors for ASD and ID. Emerging evidence highlights the critical status of these chromatin remodeling molecules in dendritic spine morphogenesis and synaptic functions. Molecular and cellular insights of ARID1B, KANSL1, and WDR5 will integrate into our current knowledge in understanding and interpreting the pathogenesis of ASD and ID. Modulation of their activities or levels may be an option for potential therapeutic treatment strategies for these neurodevelopmental conditions.
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Edited by: Sehyoun Yoon, Northwestern Medicine, United States
Reviewed by: Hiroyuki Yamazaki, Gunma University, Japan; Xin Xu, University of Alabama at Birmingham, United States
This article was submitted to Neuroplasticity and Development, a section of the journal Frontiers in Molecular Neuroscience
These authors have contributed equally to this work
ISSN:1662-5099
1662-5099
DOI:10.3389/fnmol.2022.1048713