Efnisyfirlit

• Autism
• Copyright
• Contents
• Contributors
• Preface
• Chapter One: The putative etiology and prevention of autism
• 1. Background
• 2. Glia
• 3. Astrocytes and microglia (CNS)
• 4. Oligodendrocytes (CNS)
• 5. Schwann cells (PNS)
• 6. Myelination and IGF-1
• 7. Autism etiology
• 8. Connectivity
• 9. Polymorphism and biomarkers
• 10. Autism prevention
• 11. Challenge
• Acknowledgments
• References
• Chapter Two: Role of environmental factors and epigenetics in autism spectrum disorders
• 1. Context: Genetics yes, but not only
• 2. Environmental factors
• 2.1. Maternal stress during pregnancy and ASD
• 2.1.1. Infections
• 2.1.2. Air pollutants
• 2.1.3. Organochlorides (OC) and organophosphates (OP) pesticides
• 2.1.4. Psychological stress
• 2.1.5. Anti-epileptic drug valproic acid
• 2.1.6. Folate (vitamine B9) supplementation
• 2.2. Developmental sensitivity windows
• 3. Environmental animal models for ASD
• 3.1. Anti-epileptic drug VPA rodent model
• 3.2. Maternal infections models
• 3.3. Exposure to pesticides models
• 3.4. Maternal psychological (social) stress model
• 4. Epigenetics mechanisms: The examples of valproate and folate
• 4.1. Indirectly through the γ-aminobutyric acid (GABA)-ergic system
• 4.2. Directly through the inhibition of histone deacetylase
• 4.3. The transgenerational epigenetic inheritance
• 4.4. Folate and epigenetics mechanisms
• 5. Conclusion
• References
• Chapter Three: Genomics, transcriptomics, proteomics and big data analysis in the discovery of new d
• 1. Introduction
• 2. Omics and big data studies of autism spectrum disorder
• 2.1. Immune and inflammation pathways
• 2.2. Synapse and neurodevelopment
• 2.3. Mitochondrial energy metabolism
• 2.4. Lipid transport and metabolism
• 2.5. Gut microbiome
• 2.6. Ubiquitin-proteasome system
• 2.7. Epigenetic regulation
• 2.8. Big data analysis with machine learning approach
• 3. Conclusions and future directions in the biomarker and therapy discovery based on -omics and big
• Conflict of interest
• References
• Chapter Four: Autism spectrum disorder risk prediction: A systematic review of behavioral and neural
• 1. Introduction
• 1.1. Early behavioral signs of ASD
• 1.2. Early neuroimaging derived signs of ASD
• 1.2.1. Morphological signs using structural and diffusion MRI
• 1.2.2. Neural activities with functional MRI
• 1.2.3. Neurophysiological signs measured by EEG
• 2. Methods
• 2.1. Scope of the review
• 2.2. Modalities and features
• 2.3. Analytical methods
• 3. Results
• 3.1. Screening tools
• 3.1.1. Screening tools for the general population
• 3.1.2. Screening tools for the high-risk population
• 3.2. Observational and experimental studies
• 3.3. Structural MRI
• 3.4. Functional MRI
• 3.5. EEG and ERP
• 4. Discussion
• 4.1. Summary of behavioral based prediction
• 4.2. Summary of neuroimaging based prediction
• 4.3. Issues in existing prediction studies
• 4.4. Future directions
• References
• Chapter Five: Resting-state abnormalities of posterior cingulate in autism spectrum disorder
• 1. Anatomy of the PCC
• 2. Structural connectivity of the PCC
• 3. Resting state fMRI: Intrinsic connectivity networks
• 4. The PCC as the central hub in DMN
• 5. ASD
• 6. Local resting state abnormality of the PCC in ASD
• 7. Long-range resting state abnormality of the PCC in ASD
• 8. Importance of local underconnectivity of the dorsal PCC in ASD
• 8.1. Cognitive inflexibility
• 8.2. Impaired social-emotional processing
• 9. Importance of the PCC-MPFC hypoconnectivity in ASD
• 9.1. Disturbed large-scale cortical integration
• 9.2. Impaired cognitive performance
• 9.3. Impaired social cognition
• 10. Future directions
• References
• Chapter Six: Neurobiology of sensory processing in autism spectrum disorder
• 1. Introduction
• 2. Atypical sensory processing in ASD
• 3. Vestibular system
• 4. Somatosensory system
• 5. Visual system
• 6. Auditory system
• 7. Olfactory and gustatory systems
• 8. Neuroplasticity and sensory integration
• 9. Conclusion
• Acknowledgment
• References
• Chapter Seven: The role of the endocannabinoid system in autism spectrum disorders: Evidence from mo
• 1. Animal models of autism spectrum disorder (ASD)
• 2. Understanding the etiopathology of ASD: The role of the endocannabinoid system
• 3. Alterations of ECS in animal models of ASD: Toward novel therapeutic approaches
• 4. ASD-like phenotypes induced by manipulations of the ECS: Relevance for designing animal models of
• 5. Conclusions and perspectives
• References
• Chapter Eight: The effects of oxytocin administration on individuals with ASD: Neuroimaging and beha
• 1. Introduction
• 2. Oxytocin
• 2.1. Brain-based studies of oxytocin administration in neurotypical individuals
• 3. Oxytocin and ASD
• 4. Oxytocin administration in individuals with ASD
• 4.1. Behavioral findings of oxytocin administration in individuals with ASD
• 4.2. Brain-based findings of oxytocin administration in individuals with ASD
• 5. Discussion
• 5.1. Future directions
• 6. Conclusions
• References
• Chapter Nine: Microglia in animal models of autism spectrum disorders
• 1. Introduction
• 2. Animal models of ASDs
• 2.1. Genetic animal models (Table 1)
• 2.1.1. Fmr1 (fragile X mental retardation 1)
• 2.1.2. Mecp2 (methyl-CpG binding protein 2)
• 2.1.3. Tsc1/2 (tuberous sclerosis proteins1/2)
• 2.1.4. Shank3 (SH3 and multiple ankyrin repeat domains 3)
• 2.1.5. Pten (phosphatase and tensin homolog deleted from chromosome 10)
• 2.1.6. Cntnap2 (contactin-associated protein-like 2)
• 2.1.7. Scn1a (sodium voltage-gated channel alpha subunit 1)
• 2.1.8. 15q11-13 duplicate
• 2.2. Genetic animal models targeting genes which are not related to symptomatic autism (Table 1)
• 2.2.1. Nlgn3/4 (Neuroligin3/4)
• 2.2.2. Nrx1 (neurexin1)
• 2.2.3. Shank (SH3 and multiple ankyrin repeat domains protein)
• 2.2.4. Parvalbumin
• 2.3. Animal models created by environmental manipulations (Table 2)
• 2.3.1. Valproic acid administration
• 2.3.2. Maternal immune activation
• 2.3.2.1. LPS administration
• 2.3.2.2. Poly(I:C) administration
• 3. Animal models of ASD exhibiting possible microglia involvement
• 3.1. Genetic animal models (Table 1)
• 3.1.1. Fmr1 knockout
• 3.1.2. Cx3cr1 knockout
• 3.1.3. BTBR mice
• 3.1.4. patDp/+ mice
• 3.1.5. Mecp2
• 3.2. Animal models using environmental manipulations to induce disease (Table 2)
• 3.2.1. IL-6 administration
• 3.2.2. LPS administration
• 3.2.3. Poly(I:C) administration
• 3.2.4. Air pollution
• 3.2.5. Ovalbumin administration
• 3.3. Possible animal models of ASD (Table 3)
• 3.3.1. Trem2 knockout
• 3.3.2. Atg7 knockout
• 3.3.3. CSF1-CSF1R signaling deficiency
• 3.4. Non-rodent animal models of ASDs (Table 4)
• 3.4.1. Marmoset
• 3.4.2. Pig
• 4. Treatment of ASDs by controlling microglial functions
• 5. Conclusion
• References
• Chapter Ten: The early overgrowth theory of autism spectrum disorder: Insight into convergent mechan
• 1. Introduction
• 2. The early overgrowth theory of ASD
• 3. Valproic acid and ASD
• 3.1. Epidemiological evidence
• 3.2. The VPA animal model of ASD
• 4. VPA and the cellular and molecular mechanisms of early overgrowth
• 4.1. Modulation of functional systems
• 4.1.1. Gamma-aminobutyric acid (GABA)
• 4.1.2. Glutamate
• 4.1.3. Serotonin
• 4.1.4. Dopamine
• 4.1.5. Brain-derived neurotrophic factor
• 5. Concluding remarks and future directions
• Acknowledgments
• References
• Chapter Eleven: The role of neuroglia in autism spectrum disorders
• 1. Autism spectrum disorders
• 2. Etiology of autism spectrum disorders
• 3. Molecular aspects of autism spectrum disorders
• 4. Neuroglia in autism spectrum disorders
• 4.1. Neuroglia: Homeostatic cells of the CNS
• 4.1.1. Microglia
• 4.1.2. Astrocytes
• 4.2. The role of neuroglia in autism spectrum disorders
• 4.2.1. Neuroglia and ASD genes
• 4.2.2. Neuroglia reactivity and immune response in ASD
• 4.2.3. Neuroglia and glutamate excitotoxicity in ASD
• 4.2.4. Neuroglia and environmental factors in ASD
• 4.3. Mapping neuroglia in a preclinical rodent model of ASD
• 5. Conclusions
• References
• Chapter Twelve: Oxidative stress, metabolic and mitochondrial abnormalities associated with autism s
• 1. Etiology of autism spectrum disorder
• 2. Oxidative stress and ASD
• 2.1. Where are reactive oxygen species produced?
• 2.2. Antioxidative systems
• 2.2.1. Superoxide dismutase
• 2.2.2. Catalase
• 2.2.3. Glutathione peroxidase
• 2.2.4. Glutathione
• 2.3. Oxidative stress and the brain
• 3. Metabolic abnormalities and ASD
• 3.1. The methylation cycle
• 3.2. The transsulfuration pathway
• 3.3. Abnormalities in other nutrients
• 4. Mitochondrial abnormalities and ASD
• 5. A unified framework
• 6. Comorbidity
• 7. Future treatment options
• References
• Chapter Thirteen: In vitro models for ASD-patient-derived iPSCs and cerebral organoids
• 1. Modeling human neurodevelopment in vitro
• 1.1. Pluripotent stem cells
• 1.2. Generation of PSC-derived neural cells
• 1.3. Utilizing iPSC technology in the study of ASD
• 1.3.1. Neural progenitor cells
• 1.3.2. Neurons
• 1.3.3. Glial cells
• 1.4. The progression from 2D to 3D models
• 1.5. Utilizing cerebral organoid models in the study of ASD
• 2. CRISPR/Cas9 and iPSC technologies
• 3. Limitations and future directions
• References
• Index
• Back Cover