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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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Developmental neuroscience research is on the cusp of unprecedented advances in the understanding of how variations in brain structure and function within neural circuits confer risk for symptoms of childhood psychiatric disorders. Novel dimensional approaches to illness classification, the availability of non-invasive, diverse and increasingly sophisticated methods to measure brain structure and function in humans in vivo, and advances in genetics, animal model and multimodal research now place brain-based biomarkers within reach in the field of psychiatry. These advances hold great promise for moving neuroscience research into the clinical realm. One exciting new area of translational research in child and adolescent psychiatry, is in the use of a variety of neuroscience research tools to track brain response to clinical intervention. Examples of this include: using longitudinal neuroimaging techniques to track changes in white matter microstructure following a training intervention for children with poor reading skills, or using functional imaging to compare brain activity before and after children with bipolar disorder begin taking psychotropic medication treatment. Brain stimulation is another cutting-edge research area where brain response to therapeutic intervention can be closely tracked with electroencephalography or other brain imaging modalities. Research using neuroscience tools to track brain response to clinical interventions is beginning to yield novel insights into the etiopathogenesis of psychiatric illness, and is providing preliminary feedback around how therapeutic interventions work in the brain to bring about symptom improvement. Using these novel approaches, neuroscience research may soon move into the clinical realm to target early pathophysiology, and tailor treatments to both individuals and specific neurodevelopmental trajectories, in an effort to alter the course of development and mitigate risk for a lifetime of morbidity and ineffective treatments. Excitement and progress in these areas must be tempered with safety and ethical considerations for these vulnerable populations. This research topic focuses on efforts to use neuroscience research tools to identify brain-based biomarkers of therapeutic response in child and adolescent psychiatry.

Eating Disorders --- Neuroimaging --- Affective Disorders --- Brain Stimulation --- Bipolar Disorder --- Child Psychiatry --- biomarkers --- child and youth mental health --- Neurodevelopmental disorders --- autism

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Science: general issues --- Neurosciences --- synaptic plasticity --- Synaptic Transmission --- neuronal-glial interactions --- dendritic spine --- neural circuitries formation --- Synaptic Function --- Neurodevelopmental disorders --- systems consolidation --- synaptic modulation

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Epilepsy is a neurological disorder that affects about 65 million people worldwide. Although antiepileptic drugs provide sufficient control of seizures in approximately 70% of patients with epilepsy, the remaining 30% are resistant to monotherapy. This means around 20 million people worldwide face significant adverse life-long consequences such as sudden unexpected death from epileptic seizures, increased risk of injuries, and learning and developmental disabilities at school age. That is why, a continuous search for drugs targeting novel antiseizure mechanisms and alternative ways of epilepsy management is going on. This book covers a number of valid issues aimed at understanding the etiology and pathophysiology of epilepsy, epilepsy genetics, current therapeutic challenges, and possible novel therapeutic targets. The authors point to a number of etiologic factors, which incorporate anatomic, acquired, genetic, metabolic, and immunologic aspects. The overlap between neurodevelopmental disorders and epilepsy, and the involvement of hippocampal sclerosis in the process of epileptogenesis are also elegantly described. The readers will also find a very detailed description of the contemporary management of status epilepticus. There are also clues on how to inhibit a very dangerous super refractory status epilepticus. Regarding precision medicine-based management of epilepsy, recent data on GABAA receptor variants and canonical transient receptor potential channels are provided, which can help develop novel strategies for epilepsy treatment. Ketogenic diet may be considered as a non-pharmacological option for children and adolescents suffering from drug-resistant epilepsy. The book, covering various aspects of epilepsy from receptor and genetic studies to therapeutic clues, will be of particular value to scientists and clinicians.

MJN --- Pathology of Epilepsy; Anatomical Basis of Seizures; Epilepsy Genetics; Epilepsy and Neurodevelopmental Disorders; Treatment of Status Epilepticus; CTRP Channels for Antiepileptic Drugs; GABAA Receptors in Epilepsy; Milk Nutrition in Epilepsy; Ketogenic Diet for in Epilepsy

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Women drinking during pregnancy can result in Fetal Alcohol Spectrum Disorder (FASD), which features neurodevelopmental deficit, facial dysmorphology, growth retardation, and learning disability. Research suggests the human brain is precisely shaped through an intrinsic, genetic-cellular expression that is orchestrated further upstream by an epigenetic program. This program can be influenced by environmental inputs such as alcohol. Current research suggests the genetic and epigenetics of FASD are becoming intertwined and inseparable. Now is the time for investigators to combine genetic, genomic and epigenetic alcohol research into an accessible, online platform discussion. Genetic analyses inform gene sets vulnerable to alcohol exposure during early neurulation. Prenatal alcohol exposure alters expression of gene subsets, including genes involved in neural specification, hematopoiesis, methylation, chromatin remodeling, histone variants, eye and heart development. Recently, quantitative map locusing (QTLs) that mediate alcohol-induced phenotype were identified between two mouse strains. Another question is -- besides amount, dose, and stage of alcohol exposure, why only 5% of women drinking have a newborn with FAS? Studies are also ongoing to answer this question by characterizing genome-wide expression, allele-specific expression (ASE), gene polymorphisms (SNPs) and maternal genetic factors that influence alcohol vulnerability. Alcohol exposure during pregnancy, which can lead to FASD, has been used as a model to resolve the epigenetic pathway between environment and phenotype. Epigenetics modifies genetic outputs through alteration of 3D chromatin structure and accessibility of transcriptional machinery. Several laboratories have reported altered epigenetics, including DNA methylation and histone modification, in multiple models of FASD. During development DNA methylation is dynamic, yet orchestrated as methylation progresses in a precise spatiotemporal manner during neurulation and coincides with neural differentiation. Alcohol can directly influence epigenetics through alterations of the methionine pathway and subsequent DNA or histone methylation/acetylation. Alcohol also alters noncoding RNA including miRNA and transposable elements (TEs). Evidence suggests that miRNA expression may mediate ethanol teratology, and TEs may be affected by alcohol through altering DNA methylation at LTR. In this manner epigenetic and genetics of FASD are becoming mechanistically intertwined. Can alcohol-induced epigenomic alterations be passed through generations? Early epidemiological studies revealed infants with FASD-like features in the absence of maternal alcohol, where the fathers were alcoholics. Novel mechanisms for alcohol-induced phenotypes include altered sperm DNA methylation, hypomethylated paternal allele and heritable epimutation. These studies predict heritability of alcohol-induced epigenetic abnormalities and gene functionality across generations.

Substance Abuse --- Social Welfare & Social Work --- Social Sciences --- Pregnant women --- Fetal alcohol spectrum disorders --- Children of prenatal alcohol abuse. --- Alcohol use. --- Evaluation. --- Children exposed prenatally to alcohol --- Children exposed to prenatal alcohol abuse --- Prenatal alcohol abuse victims --- Alcoholism in pregnancy --- Alcohol-related birth defects --- Alcohol-related neurodevelopmental disorders --- FASDs (Fetal alcohol spectrum disorders) --- Fetal alcohol syndrome --- Neurodevelopmental disorders, Alcohol-related --- Abnormalities, Human --- Fetus --- Syndromes --- Children of prenatal alcohol abuse --- Complications --- Diseases --- DNA Methylation --- Fetal Alcohol Syndrome --- histone modification --- Epigenetic medicine --- Genomics --- Alcoholism --- transgenerational --- Pregnancy drinking --- FASD --- Gene environmental interaction