Introductory Review on Sirtuins in Biology and Disease provides key insights for scientists and advanced students who need to understand sirtuins and the current research in this field. This book is ideal for pharmaceutical companies as they develop novel targets using sirtuins for metabolic diseases, cancer and neurodegenerative illnesses. Sirtuins are a diverse family of proteins, with several members in mammals. The functional diversity of sirtuins is rather broad, and they have been implicated in various central biological processes. Thus, they are also highly relevant in the context of various human diseases, from cancer to neurodegeneration. - Covers both the general and specific aspects of sirtuin proteins and their role in biology, aging and disease - Presents a top quality collection of leading experts who contribute on a wide range of sirtuin-related topics - Ideal resource for pharmaceutical companies as they develop novel targets using sirtuins for metabolic diseases, cancer and neurodegenerative illnesses

The enteric nervous system (ENS) is a complex neural network embedded in the gut wall that orchestrates the reflex behaviors of the intestine. The ENS is often referred to as the “little brain” in the gut because the ENS is more similar in size, complexity and autonomy to the central nervous system (CNS) than other components of the autonomic nervous system. Like the brain, the ENS is composed of neurons that are surrounded by glial cells. Enteric glia are a unique type of peripheral glia that are similar to astrocytes of the CNS. Yet enteric glial cells also differ from astrocytes in many important ways. The roles of enteric glial cell populations in the gut are beginning to come to light and recent evidence implicates enteric glia in almost every aspect of gastrointestinal physiology and pathophysiology. However, elucidating the exact mechanisms by which enteric glia influence gastrointestinal physiology and identifying how those roles are altered during gastrointestinal pathophysiology remain areas of intense research. The purpose of this e-book is to provide an introduction to enteric glial cells and to act as a resource for ongoing studies on this fascinating population of glia. Table of Contents: Introduction / A Historical Perspective on Enteric Glia / Enteric Glia: The Astroglia of the Gut / Molecular Composition of Enteric Glia / Development of Enteric Glia / Functional Roles of Enteric Glia / Enteric Glia and Disease Processes in the Gut / Concluding Remarks / References / Author Biography

Sirtuin Biology in Cancer and Metabolic Disease: Cellular Pathways for Clinical Discovery offers a compelling and thought-provoking perspective for the examination of the intriguing biology of sirtuins that ties cancer and metabolic disease together and provides a critical platform for the development of sirtuin-based novel therapeutic strategies to effectively treat cancer and metabolic disorders with precision in order to minimize any potentially detrimental clinical outcomes. An exciting prospect for the development of innovative therapeutics for cancer and metabolic disorders involves sirtuins. Sirtuins are histone deacetylases that have an intricate role in the onset and development of cancer and metabolic disease. Implementing a translational medicine format, this innovative reference highlights the ability of sirtuins to oversee critical pathways that involve stem cell maintenance, cellular proliferation, metabolic homeostasis, apoptosis, and autophagy that can impact cellular dysfunction and unchecked cellular growth that can occur during cancer and metabolic disease. Each chapter offers an intuitive perspective of advances on the application of sirtuin pathways for cancer and metabolic disease that will be become a "go-to" resource for a broad audience of scientists, physicians, pharmaceutical industry experts, nutritionists, and students. Chapters are authored by internationally recognized experts who elucidate the intimate relationship between cancer and metabolic disease that intersects with sirtuin pathways Presents the basic and clinical role of sirtuins in regard to cancer and metabolic disease Summarizes the multidiscipline views and publications for this exciting field of sirtuins for the development of new clinical treatments for cancer and metabolic disease Provides a vital foundation for a broad audience of healthcare providers, scientists, drug developers, and students in both clinical and research settings

Sirtuins in Health and Disease, Volume 154 presents the reactions catalyzed by sirtuins in terms of their unique coenzyme NAD+-dependent catalytic mechanisms, the ways to elucidate these mechanisms, and the design of the inhibitory compounds against the sirtuin-catalyzed reactions as potential therapeutic agents for human diseases. Sections cover the concepts and chemical tools in sirtuin research, SIRT4 and SIRT7, the regulatory effects of NAD metabolic pathways on sirtuin activity, sirtuins as modifiers of Huntington's Disease (HD) pathology, parasite sirtuins as targets for novel chemotherapeutic agents, targeting sirtuins – substrate specificity and inhibitor design, and chemical probes in sirtuin research. This book focuses on the outstanding issues in the sirtuin field and implications for future sirtuin research. - Presents an excellent subject, excellent structural organization, and authoritative contributions from world-renowned scholars in the sirtuin field - Provides the latest updates on sirtuins in health and disease

The book highlights work from many different labs that taught us abnormal HDACs potentially contribute to the development or progression of many human diseases including immune dysfunctions, heart disease, cancer, memory impairment, aging, and metabolic disorders.

A NEW YORK TIMES BESTSELLER “Brilliant and enthralling.”​ —The Wall Street Journal A paradigm-shifting book from an acclaimed Harvard Medical School scientist and one of Time’s most influential people. It’s a seemingly undeniable truth that aging is inevitable. But what if everything we’ve been taught to believe about aging is wrong? What if we could choose our lifespan? In this groundbreaking book, Dr. David Sinclair, leading world authority on genetics and longevity, reveals a bold new theory for why we age. As he writes: “Aging is a disease, and that disease is treatable.” This eye-opening and provocative work takes us to the frontlines of research that is pushing the boundaries on our perceived scientific limitations, revealing incredible breakthroughs—many from Dr. David Sinclair’s own lab at Harvard—that demonstrate how we can slow down, or even reverse, aging. The key is activating newly discovered vitality genes, the descendants of an ancient genetic survival circuit that is both the cause of aging and the key to reversing it. Recent experiments in genetic reprogramming suggest that in the near future we may not just be able to feel younger, but actually become younger. Through a page-turning narrative, Dr. Sinclair invites you into the process of scientific discovery and reveals the emerging technologies and simple lifestyle changes—such as intermittent fasting, cold exposure, exercising with the right intensity, and eating less meat—that have been shown to help us live younger and healthier for longer. At once a roadmap for taking charge of our own health destiny and a bold new vision for the future of humankind, Lifespan will forever change the way we think about why we age and what we can do about it.

Recent studies have indicated that epigenetic processes may play a major role in both cellular and organismal aging. These epigenetic processes include not only DNA methylation and histone modifications, but also extend to many other epigenetic mediators such as the polycomb group proteins, chromosomal position effects, and noncoding RNA. The topics of this book range from fundamental changes in DNA methylation in aging to the most recent research on intervention into epigenetic modifications to modulate the aging process. The major topics of epigenetics and aging covered in this book are: 1) DNA methylation and histone modifications in aging; 2) Other epigenetic processes and aging; 3) Impact of epigenetics on aging; 4) Epigenetics of age-related diseases; 5) Epigenetic interventions and aging: and 6) Future directions in epigenetic aging research. The most studied of epigenetic processes, DNA methylation, has been associated with cellular aging and aging of organisms for many years. It is now apparent that both global and gene-specific alterations occur not only in DNA methylation during aging, but also in several histone alterations. Many epigenetic alterations can have an impact on aging processes such as stem cell aging, control of telomerase, modifications of telomeres, and epigenetic drift can impact the aging process as evident in the recent studies of aging monozygotic twins. Numerous age-related diseases are affected by epigenetic mechanisms. For example, recent studies have shown that DNA methylation is altered in Alzheimer’s disease and autoimmunity. Other prevalent diseases that have been associated with age-related epigenetic changes include cancer and diabetes. Paternal age and epigenetic changes appear to have an effect on schizophrenia and epigenetic silencing has been associated with several of the progeroid syndromes of premature aging. Moreover, the impact of dietary or drug intervention into epigenetic processes as they affect normal aging or age-related diseases is becoming increasingly feasible.