This book addresses and synthesizes recent basic, translational, and clinical research with the goal of understanding the mechanisms behind autism spectrum disorder (ASD) and how they lead to altered brain function and behavior. Bringing clarity to these mechanisms will lead to more effective therapies for the various heterogeneous pathologies that comprise ASD. Currently there are few, if any, proven therapies for the majority of the disorders. Among the topic addressed are neural plasticity, neuroimmunology, neuroinflammation, neuroimaging, and appropriate animal and genetic models.

This book addresses and synthesizes recent basic, translational, and clinical research with the goal of understanding the mechanisms behind autism spectrum disorder (ASD) and how they lead to altered brain function and behavior. Bringing clarity to these mechanisms will lead to more effective therapies for the various heterogeneous pathologies that comprise ASD. Currently there are few, if any, proven therapies for the majority of the disorders. Topics addressed in this book include neural plasticity, neuroimmunology, neuroinflammation, neuroimaging, and appropriate animal and genetic models.

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.

Homeostatic Control of Brain Function offers a broad view of brain health and diverse perspectives for potential treatments, targeting key areas such as mitochondria, the immune system, epigenetic changes, and regulatory molecules such as ions, neuropeptides, and neuromodulators. Loss of homeostasis becomes expressed as a diverse array of neurological disorders. Each disorder has multiple comorbidities - with some crossing over several conditions - and often disease-specific treatments remain elusive. When current pharmacological therapies result in ineffective and inadequate outcomes, therapies to restore and maintain homeostatic functions can help improve brain health, no matter the diagnosis. Employing homeostatic therapies may lead to future cures or treatments that address multiple comorbidities. In an age where brain diseases such as Alzheimer's or Parkinson's are ever present, the incorporation of homeostatic techniques could successfully promote better overall brain health. Key Features include · A focus on the homeostatic controls that significantly depend on the way one lives, eats, and drinks. · Highlights from emerging research in non-pharmaceutical therapies including botanical medications, meditation, diet, and exercise. · Incorporation of homeostatic therapies into existing basic and clinical research paradigms. · Extensive scientific basic and clinical research ranging from molecules to disorders. · Emerging practical information for improving homeostasis. · Examples of homeostatic therapies in preventing and delaying dysfunction. Both editors, Detlev Boison and Susan Masino, bring their unique expertise in homeostatic research to the overall scope of this work. This book is accessible to all with an interest in brain health; scientist, clinician, student, and lay reader alike.

Autism spectrum disorder (ASD) affects approximately 1 % of the human population and is characterized by a core symptomatology including deficits in social interaction and repetitive patterns of behaviour plus various co-morbidities. Although a lot of progress has been made to uncover underlying causes and mechanisms throughout the last decade, we are still at the very beginning to understand this enormously complex neurodevelopmental condition. This special volume is focused on translational anatomy and cell biology of ASD. International experts from the field including several members of the EU-AIMS initiative launched by the European Union to develop novel treatments for ASD have contributed chapters on several topics covering all crucial aspects of translational ASD research with a special emphasis on ASD model systems including stem cells and animals. Primary objective is to clarify how anatomical and cell biological phenotypes of ASD will help to translate basic mechanisms to clinical practice and to efficiently treat affected individuals in the near future.

A comparative overview of the effects of neuropeptides on behavior, examining parallel findings in both humans and non-human animals.

More than 40 years after the official recognition of infantile autism in DSM-III, advances continue to be made in our understanding of the possible causes, assessment and evaluation, and treatment of autism spectrum disorder (ASD). With contributions by dozens of experts in the field, this second edition of the Textbook of Autism Spectrum Disorders has been updated to reflect the latest research in ASD. Unrivaled in its thoroughness, this volume discusses issues of assessment and evaluation; examines the etiology of ASD and its recognized associations with other medical conditions; analyzes standard and experimental treatments; and delves into social policy issues pertinent to individuals with ASD and those who treat them. With summary points in each chapter and copious lists of recommended readings, this is an indispensable resource for psychiatrists, psychologists, neurologists, social workers, speech therapists, educators, and all others in the continuum of care.