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ویرایش: [1st ed. 2023]
نویسندگان: Abdeslem El Idrissi (editor). Dan McCloskey (editor)
سری:
ISBN (شابک) : 3031423828, 9783031423826
ناشر: Springer
سال نشر: 2024
تعداد صفحات: 459
زبان: English
فرمت فایل : EPUB (درصورت درخواست کاربر به PDF، EPUB یا AZW3 تبدیل می شود)
حجم فایل: 19 Mb
در صورت تبدیل فایل کتاب Neurobiology of Autism Spectrum Disorders به فرمت های PDF، EPUB، AZW3، MOBI و یا DJVU می توانید به پشتیبان اطلاع دهید تا فایل مورد نظر را تبدیل نمایند.
توجه داشته باشید کتاب نوروبیولوژی اختلالات طیف اوتیسم نسخه زبان اصلی می باشد و کتاب ترجمه شده به فارسی نمی باشد. وبسایت اینترنشنال لایبرری ارائه دهنده کتاب های زبان اصلی می باشد و هیچ گونه کتاب ترجمه شده یا نوشته شده به فارسی را ارائه نمی دهد.
این کتاب یافتههای جدید هیجانانگیزی را گرد هم میآورد که ما را به درک بهتری از تغییرات اتصال عصبی در مغزهای اوتیستیک نزدیکتر میکند. این جلد به طور معتبر اپیدمیولوژی، فیزیولوژی، رشد عصبی، ژنتیک، تأثیرات محیطی، مطالعات تصویربرداری، نوروآناتومی، و نوروشیمی اختلالات طیف اوتیسم را پوشش می دهد. در حالی که نوروبیولوژی اوتیسم هنوز فاصله زیادی با درک آن دارد، این کتاب تکنیک هایی مانند استفاده از تصویربرداری مغز برای یافتن امضا در روزهای اولیه زندگی را ارائه می دهد که می تواند به حرکت در تشخیص و شناسایی مسیرهای عصبی کمک کند. درک این مکانیسم ها امکان مداخلات درمانی دارویی، رفتاری و روانی اجتماعی را فراهم می کند. با مشارکت محققان بین المللی اوتیسم، نوروبیولوژی اختلالات طیف اوتیسم مرجعی برای محققان و پزشکانی است که علاقه مند به درک نوروبیولوژی زمینه ای اختلالات طیف اوتیسم هستند.
This book brings together the exciting new findings that will bring us closer to a better understanding of the alterations of neuronal connectivity in autistic brains. This volume authoritatively covers the epidemiology, physiology, neurodevelopment, genetics, environmental influences, imaging studies, neuroanatomy, and neurochemistry of autism spectrum disorders. While the neurobiology of autism is still a long way from being understood, this book posits techniques, such as using brain imaging to find signatures in early days of life, that could help move the diagnosis and help identify neural pathways. Understanding these mechanisms opens the possibility to pharmacological, behavioral, and psychosocial therapeutic interventions. With contributions from the leading international autism researchers, Neurobiology of Autism Spectrum Disorders is the go-to reference for researchers and clinicians with an interest in understanding the underlying neurobiology of autism spectrum disorders.
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 17.2.10 Transcriptional Landscape of ASD from iPSC and Post-Mortem Studies 17.3 Conclusions and Future Directions References Chapter 18: Genes and their Involvement in the Pathogenesis of Autism Spectrum Disorder: Insights from Earlier Genetic Studies 18.1 Introduction 18.2 Genetic Studies of ASD 18.2.1 Twin Studies 18.2.2 Family Studies 18.2.3 Linkage Studies 18.2.4 Genome-Wide Association Studies 18.2.5 Cytogenetic Studies 18.2.6 Copy Number Variation (CNV) Analysis 18.3 Genes Involved in ASD Pathogenesis 18.3.1 RELN (Reelin) Gene 18.3.2 SHANK (SH3 and Multiple Ankyrin Repeat Domains Protein) Gene 18.3.3 NLGN (Neuroligin) Gene 18.3.4 OXTR (Oxytocin Receptor) Gene 18.3.5 GABR (Gamma-Aminobutyric Acid Receptor) Gene 18.3.6 MET (Mesenchymal Epithelial Transition) Gene 18.3.7 SLC6A4 (Solute Carrier Family 6 Member 4) Gene 18.3.8 SLC25A12 (Solute Carrier Family 25 Member 12) Gene 18.3.9 MAO (Monoamine Oxidase) Gene 18.3.10 ITGB3 (Integrin-β 3) Gene 18.4 Concluding Remarks References Chapter 19: Electrophysiology of Semantic Processing in ASD 19.1 Electrophysiology of Semantic Processing in Healthy Population 19.2 Classic ERPs Components Associated with Semantic Processing 19.2.1 N400 19.2.2 Later Positivities 19.2.3 Later Sustained Negativity 19.3 Electrophysiology of Semantic Processing in ASD 19.3.1 Semantic Processing of Verbal Information 19.3.2 Semantic Processing of Visual Information 19.3.3 Semantic Processing of Cross-Modal Information 19.4 Oscillatory Activation 19.4.1 Future Directions 19.4.1.1 The Visual Ease Assumption References Chapter 20: Gestational Exposure to Di-n-Butyl Phthalate Induces Autism-Like Behavior Through Inhibition of Neuro-Steroidogenesis 20.1 Introduction 20.2 Materials and Methods 20.2.1 Animals 20.2.2 High-Performance Liquid Chromatography (HPLC) 20.2.3 Western Blotting 20.2.4 Immunohistochemical Analysis 20.2.5 cDNA Preparation and Quantitative Real-Time PCR Analysis 20.2.6 Scanning Electron Microscopy 20.2.7 Statistical Analysis 20.2.8 Results 20.2.8.1 DBP Levels in the Brain of Offspring 20.2.8.2 Gestational Exposure to DBP Disrupts Key Proteins in Steroidogenesis 20.2.8.3 Gestational Exposure to DBP Reduces the Expression of Steroidogenic and GABAergic Proteins 20.2.9 Discussion References Index