Abstract

Autism spectrum disorder (ASD) is an umbrella term encompassing several neurodevelopmental disorders such as Asperger syndrome or autism. It is characterised by the occurrence of distinct deficits in social behaviour and communication and repetitive patterns of behaviour. The symptoms may be of different intensity and may vary in types. Risk factors for ASD include disturbed brain homeostasis, genetic predispositions, or inflammation during the prenatal period caused by viruses or bacteria. The number of diagnosed cases is growing, but the main cause and mechanism leading to ASD is still uncertain. Recent findings from animal models and human cases highlight the contribution of glia to the ASD pathophysiology. It is known that glia cells are not only “gluing” neurons together but are key players participating in different processes crucial for proper brain functioning, including neurogenesis, synaptogenesis, inflammation, myelination, proper glutamate processing and many others. Despite the prerequisites for the involvement of glia in the processes related to the onset of autism, there are far too little data regarding the engagement of these cells in the development of ASD.

Highlights

  • Autism spectrum disorder (ASD) is a set of neurodevelopmental disorders characterised by reduced sociability, problems with communication, repetitive patterns of behaviour and co-morbid features, including cognitive impairments

  • Findings from this study have shown the potential role for astrocytes in ASD pathogenesis, as well as identified ATP as a new potential molecular player in ASD, confirming the synaptopathy hypothesis of autism

  • Experimental data regarding the role of inflammatory processes, disturbed synaptogenesis and neurogenesis in the occurrence of autism spectrum disorder allow to hypothesise that disruption of normal glia function, which are the main players in exactly these processes, may underlie the occurrence of ASD or contribute to worsening or/and improvement of autistic symptoms

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Summary

Introduction

ASD is a set of neurodevelopmental disorders characterised by reduced sociability, problems with communication, repetitive patterns of behaviour and co-morbid features, including cognitive impairments. Because ASD is a complex neurodevelopmental disorder, animal environmental models are usually based on the exposure of pregnant rodents to certain drugs to disturb the normal development of offspring. Another factor linked to the onset of ASD is the activation of the maternal immune system. There is plenty of evidence for autism-associated brain impairments such as disturbed synaptogenesis, altered number of synapses, imbalance between excitation and inhibition, perturbed neuronal differentiation, improper cortex lamination, and increase and decrease in the amount of parvalbumin-, or calbindin-positive cells in the cortex, striatum and hippocampi in animal models of ASD [12,13]

Different Models of ASD
Symptoms of ASD in Animal Models Behaviour Associated with Social Skills
Anatomical and Neuronal Changes in ASD
Astrocytes as Important Players in the CNS
Astrocytes in ASD—Insights from the Clinical Cases and Preclinical Models
Astrocytes and Metabolism
Impaired Calcium Signalling in Astrocytes—Influence on ASD
Oligodendroglia and Their Precursors
Findings
Conclusions
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