Neurobiology of Autism Spectrum Disorders

• Autore: El Idrissi Abdeslem
• Pubblicazione: Cham : , : Springer International Publishing AG, , 2024; ©2023
• Edizione: 1st ed.
• Descrizione fisica: 1 online resource (448 pages)
• Disciplina: 616.85882
• Soggetto topico: Neurobiologia; Trastorns de l'espectre autista
• Soggetto genere / forma: Llibres electrònics
• Altri autori: McCloskeyDan
• Nota di contenuto: Intro -- Preface -- Contents -- Chapter 1: Dysfunctional Circuit Mechanisms of Sensory Processing in FXS and ASD: Insights from Mouse Models -- 1.1 Sensory Processing and Decision Making -- 1.2 Fragile X Syndrome -- 1.3 Mouse Models of Fragile X Syndrome and ASD -- 1.4 Sensory Processing Deficits in the Context of Impaired Inhibition -- 1.5 Inhibition in the Neurotypical Sensory Cortex -- 1.6 Sensory Deficits in the Visual Domain -- 1.6.1 Humans -- 1.6.2 Mice -- 1.7 Sensory Deficits in the Auditory Domain -- 1.8 Sensory Deficits in Somatosensory Domain -- 1.9 Conclusion -- References -- Chapter 2: Theory of Mind in Autism -- 2.1 Introduction -- 2.2 Critical and Landmark Studies of ToM -- 2.2.1 Premack and Woodruff (1978) -- 2.2.2 Perner and Wimmer (1983) -- 2.2.3 Baron-Cohen, Leslie, and Frith (1985) -- 2.2.4 Mirror-Neuron Research -- 2.2.5 Studies to Investigate Precursors or Prerequisites of ToM -- 2.3 A Challenge to Study Theory of Mind: The Problem of Investigating the Unobservable in Science -- 2.4 Conclusion -- References -- Chapter 3: Prenatal and Early Life Environmental Stressors: Chemical Moieties Responsible for the Development of Autism Spectrum Disorder -- 3.1 Introduction -- 3.2 Prenatal/Perinatal Exposure to Environmental Stressors -- 3.2.1 Valproic Acid -- 3.2.2 Hyperserotonemia -- 3.2.3 Maternal Infections -- 3.2.4 Endocrine Disruptors -- 3.2.4.1 Polychlorinated Biphenyls -- 3.2.4.2 Bisphenol - A -- 3.2.5 Pesticides -- 3.2.6 Heavy Metals -- 3.2.7 Nutritional Deficiency -- 3.2.7.1 Vitamin D -- 3.2.7.2 Amino Acids -- 3.2.7.3 B-Vitamins -- 3.3 Conclusion -- References -- Chapter 4: Animal Models of ASD -- 4.1 Non-genetic Animal Models -- 4.2 Genetic Animal Models -- 4.3 Conclusion -- References -- Chapter 5: Mitochondrial Dysfunction in Autism Spectrum Disorders -- 5.1 Introduction -- 5.2 Etiology and Pathophysiology of ASD. ; 5.3 Mitochondrial Dysfunction in ASD -- 5.3.1 Mitochondrial Dysfunction in the Brain of ASD Subjects -- 5.3.2 Alterations in Mitochondrial DNA in ASD Subjects -- 5.3.3 Brain Oxidative Stress in ASD -- 5.4 Conclusion -- References -- Chapter 6: The Usability of Mouse Models to Study the Neural Circuity in Autism Spectrum Disorder: Regulatory Mechanisms of Core Behavioral Symptoms -- 6.1 Current Trends in ASD Studies Using Animal Models -- 6.2 Assessment of Atypical Social Behavior in Animal Models -- 6.3 Neural Circuits Responsible for the Regulation of ASD-Like Behavior -- 6.4 Peptide Hormones Regulating Complex Social Behavior -- 6.5 OXT-Mediated Neural Circuits -- 6.6 AVP-Mediated Neural Circuits -- 6.7 Concluding Remarks -- References -- Chapter 7: Seizures in Mouse Models of Autism -- 7.1 Sex Bias of Presentation of ASD and Epilepsy -- 7.2 Early Epileptic Activity and ASD -- 7.3 Imbalance of Excitation and Inhibition as a Common Etiology for ASD and Epilepsy -- 7.4 Seizures in Monogenetic Mouse Models of ASD -- 7.4.1 16p11.2 -- 7.4.2 ARID1B -- 7.4.3 CACNA1C -- 7.4.4 CNTNAP2 -- 7.4.5 CUL3 -- 7.4.6 DYRK1A -- 7.4.7 GTF2I -- 7.4.8 RAI1 -- 7.4.9 SHANK3 -- 7.4.10 SYNGAP1 -- 7.4.11 UBE3A -- 7.5 Conclusions -- References -- Chapter 8: Lipid-Related Pathophysiology of ASD -- 8.1 Lipids Are Essential to Biomechanisms -- 8.1.1 Lipids in the Periphery -- 8.1.1.1 Cholesterol Transport and Lipoproteins -- 8.1.1.2 Lipoproteins Transport Materials Including Steroids and miRNA -- 8.1.2 Lipids in the CNS -- 8.1.2.1 Cholesterol Production in the Brain -- 8.1.2.2 Cholesterol's Role in Development -- 8.1.2.3 Cholesterol's Role in Signaling -- 8.1.2.4 Cholesterol's Role in Synaptic Function -- 8.1.2.5 Other Lipids in the Brain -- 8.2 Lipid-Related Abnormalities Have Been Found in ASD-Related Genetic Disorders -- 8.2.1 Smith-Lemli-Opitz Syndrome. ; 8.2.2 Fragile X Syndrome -- 8.2.3 Rett Syndrome -- 8.3 Lipid Disorders with Known Genetic Variants Not Associated with ASD -- 8.3.1 Post-Squalene Disorders Involved with Cholesterol Biosynthesis -- 8.3.2 Hypoapolipoprotein Disorders: Hypoalphalipoproteinemia, Hypobetalipoproteinemia, Abetalipoproteinemia, and Familial Combined Hypolipidemia -- 8.3.3 Hyperlipidemic Disorders Caused by Variants in Genes That Also Cause Hypolipidemic Disorders -- 8.4 Lipid Abnormalities Associated with ASD that Are Not Observed with Known Genetic Disorders -- References -- Chapter 9: Perinatal Insulin-Like Growth Factor as a Risk Factor for Autism -- 9.1 Introduction -- 9.2 Methods -- 9.3 Results/Discussion -- 9.3.1 Conclusions -- References -- Chapter 10: Prophylactic Treatment of ASD Based on Sleep-Wake Circadian Rhythm Formation in Infancy to Early Childhood -- 10.1 Introduction -- 10.2 Circadian Rhythm Formation -- 10.3 Age-related Changes in Sleep Development -- 10.3.1 Sleep Duration -- 10.3.2 Sleep Characteristics of Children with ASD -- 10.3.3 Night Awakening (Sleep Fragmentation) -- 10.3.4 Difference in Sleep Duration Between Weekdays and Weekends -- 10.3.5 Social Jet Lag Tendency of Infants and Young Children -- 10.4 Appropriate Period of Nocturnal Sleep -- 10.5 Direction of ASD Treatment -- 10.6 Appropriate Age for Treatment -- 10.7 Therapy for Sleep Disorders in Infancy to Early Childhood -- 10.7.1 Sleep Hygiene -- 10.7.1.1 Sleep-Wake Rhythm Adjustment -- 10.7.1.2 Awakening During Night -- Discontinuing (Breast) Feeding at Night (Fig. 10.5) -- 10.7.2 Pharmacotherapy (Figs. 10.6, 10.7 and 10.8) -- 10.7.2.1 Delayed Sleep Onset (Sleep Onset Insomnia) -- Melatonin -- Clonidine -- Benzodiazepine -- Triclofos Sodium(TFS) -- 10.7.2.2 Awakening (Sleep Fragmentation) -- Antihistamine -- Risperidone -- 10.7.3 Hospitalization -- 10.8 Summary -- References. ; Chapter 11: Imbalances of Inhibitory and Excitatory Systems in Autism Spectrum Disorders -- 11.1 The Excitation/Inhibition Imbalance Model and Autism -- 11.2 Clinical Evidence for E/I Imbalance in ASD -- 11.3 Links Between E/I Imbalance and Autism-Like Behavior in Model Systems -- 11.4 Implications for Therapeutic Treatments Targeting E/I Imbalance -- References -- Chapter 12: Shared Developmental Neuropathological Traits Between Autism and Environmental Lead Exposures: Insights into Convergent Sulfur-Dependent Neurobiological Mechanisms -- 12.1 Brief Literature Review of the Last Decade -- 12.2 Glutathione as a Shared Neurobiological Target for Understanding Late-to-Early Neurodevelopmental Disorders and Its Implications on the GABA-Shift -- 12.3 Lead Poisoning and Autism Alter Brain Glutathione Levels -- 12.4 Understanding the Physical Chemistry Between Lead and Sulfur Compounds -- 12.5 Sulfur-Dependent Approaches for Ameliorating Lead Poisoning and Autism: Taurine Neuroprotection Through Glutathione -- 12.6 Discussion and Conclusions -- References -- Chapter 13: Epidemiological Surveys of ASD: Current Findings and New Directions -- 13.1 Introduction -- 13.2 Review of Prevalence Surveys -- 13.3 Special Issues -- 13.3.1 Case Definition and Case Status Determination -- 13.3.2 The Problems of Parental Reports -- 13.3.3 Novel Approaches to Case Finding/Ascertainment -- 13.3.4 Worldwide Studies and Cultural Issues -- 13.3.5 Surveillance -- 13.4 Conclusions -- References -- Chapter 14: Metabolic Approaches to the Treatment of Autism Spectrum Disorders -- 14.1 Vitamins -- 14.1.1 Vitamin B1 -- 14.1.2 Vitamin B2 -- 14.1.3 Vitamin B3 -- 14.1.4 Vitamin B5 -- 14.1.5 Vitamin B6 -- 14.1.6 Vitamin B7 -- 14.1.7 Vitamin B9 -- 14.1.8 Vitamin B12 -- 14.1.9 Vitamin C -- 14.1.10 Vitamin A -- 14.1.11 Vitamin D -- 14.1.12 Vitamin E -- 14.2 Minerals -- 14.2.1 Zinc. ; 14.2.2 Magnesium -- 14.2.3 Lithium -- 14.2.4 Molybdenum -- 14.3 Other Nutrients -- 14.3.1 Omega-3 Fatty Acids -- 14.3.2 N-acetyl Cysteine -- 14.3.3 Coenzyme Q10 -- 14.3.4 Alpha-Lipoic Acid -- 14.3.5 Creatine Monohydrate -- 14.3.6 Sulforaphane -- 14.3.7 Melatonin -- 14.3.8 Carnitine -- 14.3.9 Tetrahydrobiopterin -- 14.4 Dietary Interventions with a Metabolic Approach -- 14.4.1 Ketogenic Dietary Therapies -- 14.5 Summary and Conclusions -- References -- Chapter 15: Autism and Neurodiversity -- 15.1 Heterogeneity in Autism -- 15.2 What Is Neurodiversity -- 15.3 Medical Model -- 15.3.1 Historical Medical Model -- 15.3.2 Modern Medical Model -- 15.4 Social Model of Disability -- 15.5 Ecological Model of Neurodiversity -- 15.6 Indigenous Models of Neurodiversity -- 15.7 Major Autism Movements -- 15.8 Unifying View of Autism with Combined Models -- 15.9 Recommendations for Biological Studies of Autism -- 15.10 Conclusion -- References -- Chapter 16: Principal Findings of Auditory Evoked Potentials in Autism Spectrum Disorder -- 16.1 Introduction -- 16.2 Evidence of Neurophysiological Abnormalities with ABR in ASD -- 16.3 Evidence of Neurophysiological Abnormalities with LLAEP in ASD -- 16.4 Conclusion -- References -- Chapter 17: Developmental Origins of the Structural Defects Implicated in ASD: Insights from iPSC and Post-Mortem Studies -- 17.1 Introduction -- 17.1.1 2D and 3D iPSC Models -- 17.1.2 The Need for an Integrated Approach -- 17.2 Complementary Findings in iPSC and Postmortem Studies of ASD -- 17.2.1 Brain Size and Neuronal Numbers -- 17.2.2 Proliferation and Neurogenesis -- 17.2.3 Differentiation and Cell-Type Comittment -- 17.2.4 Apoptosis -- 17.2.5 Cortical Cytoarchitecture -- 17.2.6 Neuropathological Alterations in Morphology and Synapses -- 17.2.7 Excitatory/Inhibitory (E/I) Imbalance -- 17.2.8 Reelin (RELN) Dysfunction. ; 17.2.9 Gliogenesis.
• Titolo autorizzato: Neurobiology of Autism Spectrum Disorders
• ISBN: 3-031-42383-6
• Formato: Materiale a stampa
• Livello bibliografico: Monografia
• Lingua di pubblicazione: Inglese
• Record Nr.: 9910835064903321
• Lo trovi qui: Univ. Federico II