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Nowadays, neurodevelopmental disorders comprise a large proportion of mental health diagnoses. These disorders, according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, include intellectual disabilities, communication disorders, autism spectrum disorders, attention deficit hyperactivity disorders, specific learning disorders, and motor disorders. Current research is pointing in the direction of schizophrenia, bipolar disorders, and other disorders being included in the category of neurodevelopmental disorders as well. There is a great deal of overlap among these disorders and they are best understood in a dimensional fashion. This book sets out the future of psychiatry in relation to these disorders and what is basically a new understanding of psychiatry in recent decades. Chapters cover topics such as early recognition of schizophrenia, epilepsy, and the genetics of ataxia telangiectasia. Also included is an examination of the complex issue of systems biology and neurodevelopment.
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Nowadays, neurodevelopmental disorders comprise a large proportion of mental health diagnoses. These disorders, according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, include intellectual disabilities, communication disorders, autism spectrum disorders, attention deficit hyperactivity disorders, specific learning disorders, and motor disorders. Current research is pointing in the direction of schizophrenia, bipolar disorders, and other disorders being included in the category of neurodevelopmental disorders as well. There is a great deal of overlap among these disorders and they are best understood in a dimensional fashion. This book sets out the future of psychiatry in relation to these disorders and what is basically a new understanding of psychiatry in recent decades. Chapters cover topics such as early recognition of schizophrenia, epilepsy, and the genetics of ataxia telangiectasia. Also included is an examination of the complex issue of systems biology and neurodevelopment.
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Nowadays, neurodevelopmental disorders comprise a large proportion of mental health diagnoses. These disorders, according to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, include intellectual disabilities, communication disorders, autism spectrum disorders, attention deficit hyperactivity disorders, specific learning disorders, and motor disorders. Current research is pointing in the direction of schizophrenia, bipolar disorders, and other disorders being included in the category of neurodevelopmental disorders as well. There is a great deal of overlap among these disorders and they are best understood in a dimensional fashion. This book sets out the future of psychiatry in relation to these disorders and what is basically a new understanding of psychiatry in recent decades. Chapters cover topics such as early recognition of schizophrenia, epilepsy, and the genetics of ataxia telangiectasia. Also included is an examination of the complex issue of systems biology and neurodevelopment.
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Describing the clinical aspects of the most common neurodevelopmental disorders, including autism and ADHD, for psychiatrists and other clinicians working in forensic services, this title covers policy, legal issues, assessment, therapeutic approaches and pathways through the criminal justice system.
Forensic neuropsychology. --- Developmental disabilities --- Social aspects. --- Neurodevelopmental Disorders --- Forensic Psychiatry
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The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.
Cerebellum --- Striatum --- Oxytocin --- mTOR --- Hypothalamus --- Neurodevelopmental disorders --- Cell signaling
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The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.
Cerebellum --- Striatum --- Oxytocin --- mTOR --- Hypothalamus --- Neurodevelopmental disorders --- Cell signaling
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The Centers for Disease Control and Prevention estimate that 1 in 68 children in the United states is afflicted with autism spectrum disorders (ASD), yet at this time, there is no cure for the disease. Autism is characterized by delays in the development of many basic skills, most notably the ability to socialize and adapt to novelty. The condition is typically identified in children around 3 years of age, however the high heritability of autism suggests that the disease process begins at conception. The identification of over 500 ASD risk genes, has enabled the molecular genetic dissection of the pathogenesis of the disease in model organisms such as mice. Despite the genetic heterogeneity of ASD etiology, converging evidence suggests that these disparate genetic lesions may result in the disruption of a limited number of key biochemical pathways or circuits. Classification of patients into groups by pathogenic rather than etiological categories, will likely aid future therapeutic development and clinical trials. In this set of papers, we explore the existing evidence supporting this view. Specifically, we focus on biochemical cascades such as mTOR and ERK signaling, the mRNA network bound by FMRP and UBE3A, dorsal and ventral striatal circuits, cerebellar circuits, hypothalamic projections, as well as prefrontal and anterior cingulate cortical circuits. Special attention will be given to studies that demonstrate the necessity and/or sufficiency of genetic disruptions (e.g. by molecular deletion and/or replacement) in these pathways and circuits for producing characteristic behavioral features of autism. Necessarily these papers will be heavily weighted towards basic mechanisms elucidated in animal models, but may also include investigations in patients.
Cerebellum --- Striatum --- Oxytocin --- mTOR --- Hypothalamus --- Neurodevelopmental disorders --- Cell signaling --- Cerebellum --- Striatum --- Oxytocin --- mTOR --- Hypothalamus --- Neurodevelopmental disorders --- Cell signaling
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Endocrine disrupting chemicals --- Endocrine glands --- Endocrine Disruptors --- Environmental Exposure --- Neurotoxins --- Neurosecretory Systems --- Neurodevelopmental Disorders --- Risk Assessment
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Child Psychiatry. --- Neurodevelopmental Disorders. --- Child psychiatry --- Enfants --- Case studies --- Psychiatrie --- Cas, Etudes de
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Fetal alcohol spectrum disorders. --- Alcohol-related birth defects --- Alcohol-related neurodevelopmental disorders --- FASDs (Fetal alcohol spectrum disorders) --- Fetal alcohol syndrome --- Neurodevelopmental disorders, Alcohol-related --- Abnormalities, Human --- Alcoholism in pregnancy --- Fetus --- Syndromes --- Children of prenatal alcohol abuse --- Complications --- Diseases
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