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This book comprehensively reviews the proteins associated with neurodevelopmental disorders, including autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD). It also discusses the interactions of the associated-proteins, like bromodomain-containing proteins (BCPs), kinases, synaptic proteins, scaffolding proteins, transcriptional factors, and DNA-binding proteins at the subcellular and molecular levels. The book also explores the potential of these proteins as a druggable target and a biomarker in the neurodevelopmental disorders. The book further explores the recent advancements in understanding the important role of epigenetic factors in predisposition to these diseases. Lastly, it presents genetic factors that lead to variation in gene expression in these diseases, disorders management via diet intervention and the future potential of stem cell therapy.
Neurodevelopmental Disorders, the latest release in the Comprehensive Developmental Neuroscience series, presents the most thorough coverage available, addressing all aspects on how the nervous system and its components develop. This book brings together the latest research in this rapidly evolving field, with section editors discussing the technological advances that are enabling the pursuit of new research on brain development. This volume focuses on neurodevelopmental disorders in humans and experimental organisms. Particular attention is paid to the effects of abnormal development and on new psychiatric/neurological treatments being developed based on our increased understanding of developmental mechanisms. - Features leading experts in various subfields as section editors and article authors - Presents articles that have been peer reviewed to ensure accuracy, thoroughness and scholarship - Covers disorders of the nervous system that arise through defects in neural development
Recent years have seen spectacular advances in the field of circadian biology. These have attracted the interest of researchers in many fields, including endocrinology, neurosciences, cancer, and behavior. By integrating a circadian view within the fields of endocrinology and metabolism, researchers will be able to reveal many, yet-unsuspected aspects of how organisms cope with changes in the environment and subsequent control of homeostasis. This field is opening new avenues in our understanding of metabolism and endocrinology. A panel of the most distinguished investigators in the field gathered together to discuss the present state and the future of the field. The editors trust that this volume will be of use to those colleagues who will be picking up the challenge to unravel how the circadian clock can be targeted for the future development of specific pharmacological strategies toward a number of pathologies.
This volume explores the latest techniques used to study neurodevelopmental diseases (NDD) that range from molecular aspects to integrated research approaches and brain imaging in living rodents. Chapters in this book cover topics such as protocols to deliver shRNA in vitro and in vivo using lentiviral particles to knock-down specific protein expression; experimental procedures to use recombinant fluorescent probes to visualize endogenous proteins at the mammalian synapse; CRISPR/Cas9 toolkit to assess either gain- or loss-of-gene function in brain organoids; detailed protocols to use in vivo manipulations to correct the behavioral phenotypes in cognitive disorder mouse lines; and experimental approaches to genetically engineer macaque models of NDDs and investigate how genetic predisposition may cause neural and functional alterations. In the Neuromethods series style, chapters include the kind of detail and key advice from the specialists needed to get successful results in your laboratory. Cutting-edge and practical, Translational Research Methods in Neurodevelopmental Disorders is a valuable resource for all researchers who want to learn more about this important and developing field.
The development of the human brain is a vastly complex process resulting in an elaborate network of over one hundred billion neurons, with each neuron having thousands of synaptic connections. The proper organization of these cells and the formation of their processes is essential for the construction of a functional brain. Disruptions in this process result in a number of developmental disorders; including, epilepsy and autism spectrum disorder (ASD). 17p13.3 microduplication syndrome is a newly identified genetic disorder resulting in a variety of defects including ASD. Importantly, a minimum duplication region strongly associated with ASD has been classified and exclusively contains the gene encoding the protein 14-3-3[epsilon], strongly implicating the overexpression of 14-3-3[epsilon] in ASD. Using in vitro and in vivo techniques, we have found that 14-3-3[epsilon] binds to the microtubule binding protein doublecortin, preventing its degradation resulting in increased doublecortin protein levels. We also found that 14-3-3[epsilon] overexpression disrupts neurite formation by preventing the invasion of microtubules into primitive neurites, which can be rescued by the knockdown of doublecortin. Our findings provide the first evidence of cellular pathology in 17p13.3 microduplication syndrome. In addition the functions of 14-3-3[epsilon] in cortical development, in this work we have also analyzed the role of 14-3-3[gamma], another 14-3-3 isoform. Williams Syndrome (WS) is a neurodevelopmental disorder caused by deletions in the 7q11.23 chromosome locus resulting in intellectual disabilities. Typical WS patients present a 1.5-1.8Mb deletion whereas atypical patients have a larger than 1.8 Mb deletion, which includes the gene encoding 14-3-3[gamma]. Interestingly, atypical WS patients commonly exhibit epilepsy. Furthermore, there is a reciprocal duplication syndrome to WS, which also results in epilepsy and intellectual disabilities. Taken together with the fact that defects in neuronal migration typically result in epilepsy, we analyzed if the overexpression and knockdown of 14-3-3[gamma] causes neuronal migration defects. We found that the overexpression and the knockdown of 14-3-3[gamma] in utero results in delays in neuronal migration due to decreased neuronal migration velocity. Furthermore, we found no defects in neurogenesis when 14-3-3[gamma] levels are altered. These results indicate that balanced expression of 14-3-3[gamma] is required for proper neuronal migration.
Neurodevelopmental disorders arise from disturbances to various processes of brain development, which can manifest in diverse ways. They encompass many rare genetic syndromes as well as common, heritable conditions such as intellectual disability, autism, ADHD, schizophrenia and many types of epilepsy. The Genetics of Neurodevelopmental Disorders examines recent revolutionary advances in our understanding of the genetics of these disorders, exploring both basic discoveries and the translation of new findings into the clinical setting. The book begins by examining the genetic architecture and etiology of neurodevelopmental disorders. It describes the striking recent progress in identifying pathogenic mutations, which are grouped here based on the neurodevelopmental processes impacted. Subsequent chapters consider the use of cellular and animal models to elucidate the cascading consequences of such mutations, from molecular and cellular levels to emergent effects on neural circuits, brain systems and subsequent psychological development. The text concludes by examining the important clinical implications of the recent advances in the field, from recognition of the genetic causes in individual patients to development of new treatments and interventions. A timely synthesis, The Genetics of Neurodevelopmental Disorders is a unique and essential resource for neuroscientists, geneticists, neurologists and psychiatrists and an accessible and up-to-date overview for medical and science students.
Autism spectrum disorders are developmental disorders. Individuals with autism spectrum disorders develop differently. These differences are usually present in social interaction, communication, and sensory processing, and become visible through a wide variety of behavioral responses that differ from individuals without autism spectrum disorders. Despite significant research efforts, the exact causes of autism spectrum disorders remain poorly understood; however, researchers have gained extensive insights into possible pathomechanisms, even at the molecular level of cells. Many diagnostic criteria have been developed, adapted, and improved. The eight chapters in this book highlight the current state-of-the-art in many areas of autism spectrum disorders. Chapter 1 provides an overview of the epidemiology of autism spectrum disorders and the current knowledge of the underlying pathogenic mechanisms. Chapter 2 summarizes the diagnostic criteria and procedures and highlights present and upcoming therapeutic strategies. Chapter 3 reviews the adverse events and trauma in people with autism spectrum disorders. Chapters 4 and 5 focus on atypical sensory processing, and Chapter 6 discusses the genetic overlap of autism spectrum disorders with other neuropsychiatric disorders such as attention deficit hyperactivity disorder (ADHD), depression, and schizophrenia. Chapter 7 focuses on the contribution of abnormalities in mitochondria, and chapter 8 discusses gut-brain interactions and a potential role for microbiota in autism spectrum disorders. This book is aimed primarily at clinicians and scientists, but many areas will also be of interest to the layperson.