Mark P. Mattson - Böcker

NOT JUST FOR WEIGHT LOSS: A neuroscientist explores the science and history of intermittent fasting, revealing the wide-ranging mental and physical benefits of this time-tested eating pattern.Most of us eat 3 meals a day with a smattering of snacks because we think that’s the normal, healthy way to eat. But when we look at the eating patterns of our distant ancestors, we can see that an intermittent fasting eating pattern is normal—and eating 3 meals a day is not. In The Intermittent Fasting Revolution, prominent neuroscientist Mark Mattson shows that frequent periods of time with little or negligible amounts of food is not only normal but also good for us. He describes the specific ways intermittent fasting can: • Enhance our ability to cope with stress by making cells more resilient• Improve mental and physical performance• Slow aging and reduce the risk of diseases like obesity, Alzheimer’s, and diabetesMattson—whose pioneering research uncovered the ways that the brain responds to fasting and exercise—explains how thriving while fasting became an evolutionary adaptation; it’s not just the latest fad diet for weight loss. He also offers practical advice on adopting an intermittent fasting eating pattern as well as information for parents and physicians.

Apoptosis, or programmed cell death, is an adaptive form of cell death that plays a critical role in turnover of mitotic cells and various tissues in the adult, including epithelial cells, fibroblasts and various endocrine cells. Programmed cell death also plays a major role in development in organizing the body plan and molding intricate cellular structures such as nerve cell circuits in the brain. Rapidly progressing research into the molecular and biochemical underpinnings of the programmed cell death process are revealing novel genetic programs and molecular interactions that coordinate a process that results in death and removal of cells without an immune response and in the absence of the adverse effects on neighboring cells.

Programmed Cell Death, Volume I, critically details the molecular, biochemical and cellular mechanisms of apoptosis. This volume covers programmed cell death in a variety of tissues and organ systems highlighting the interesting families of proteins involved in promoting or preventing apoptosis. These include the caspase and calpain families of proteases, Bcl-2 family members, and inhibitors of apoptosis proteins. Each chapter is written by an internationally recognized expert in a particular aspect of programmed cell death.

This book will provide the reader with a comprehensive understanding of the cascade of events leading from an apoptotic signal, such as trophic factor withdrawal or increased oxidative stress, to cell death. Importantly, this volume also covers signaling mechanisms designed to prevent apoptosis. Such anti-apoptotic signaling cascades involve neurotrophic factors and stress response pathways. Programmed Cell Death, Volume I, provides the molecular and cellular foundation for http://www.elsevier.com/locate/isbn/0444507302Programmed Cell Death, Volume II in which the roles of aberrant regulation of apoptosis in human diseases ranging from cancer to Alzheimer's disease are considered.

Collectively, the chapters in this work will provide the reader with novel insight into the inter-relationships of the function of different organelles in the sequences of events that lead to cellular dysfunction and degeneration in the aging human population. The chapters are rich in information for cell and molecular biologists pursuing studies of the different diseases covered. In addition, the clinician will find value in understanding mechanisms underlying age-related disease as such an understanding will lead to novel therapeutic approaches for an array of age-related diseases.

This volume of Advances in Cell Aging and Gerontology critically reviews the rapidly advancing area of telomerase research with a focus at the molecular and cellular levels. The clearly established function of telomerase is to maintain chromosome ends during successive rounds of cell division by adding a six base DNA repeat on to the telomeric ends of chromosomes. As presented in the chapters of this volume, the mechanisms that regulate telomerase expression and activity are complex. Moreover, emerging data suggest additional roles for telomerase in the regulation of cell differentiation and survival.

It is expected that this quite comprehensive volume will provide a valuable resource for graduate students and postdocs in the telomerase field and for established investigators in other fields who are beginning to study telomerase in their particular research program. With an increasing number of proteins being brought into the fold of telomerase research (e.g., DNA damage and repair response proteins, heat-shock proteins, and proteins in various signal transduction cascades) many new scientists are beginning to study this enzyme from novel vantage points.

Prominent researchers and clinicians dissect the signaling pathways of an array of neuroprotective factors, ranging from neurotrophins (NGF, BDNF, NT-3, and NT-4/5) to growth factors (bFGF, IGF-1, GDNF), to cytokines (TNF, IL-1b, and TGFb), to secreted amyloid precursor proteins, to protease nexin-1. Also treated are cytoprotective signaling events that occur with injured neurons independently of intercellular signals. In elucidating the molecular cascades evolved by the nervous system to protect itself, the contributors lay the basis for powerful new drug discovery and gene therapy strategies, and shed light on potential effective strategies for preventing neuron degeneration in such conditions as stroke, traumatic brain injury, Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis.

In this groundbreaking book, leading experts detail the cellular and molecular cascades that cause selective degeneration of neuronal populations, and illuminate those genetic and environmental factors that are critical to the facilitation or suppression of the neuropathologic processes. Working from studies of human patients, as well as from cell culture and animal models, the authors demonstrate a heretofore unrecognized convergence of the causative pathogenetic mechanisms for clinically distinct neurological disorders. At center stage are the biochemical and molecular cascades that will ultimately lead to neuronal death - cascades involving oxyradical production, aberrant regulation of cellular ion homeostasis, activation of specific proteases, and activation of a stereotyped sequence of events involving mitochondial dysfunction. Individual chapters examine how these mechanisms - along with genetic and environmental factors - operate in Alzheimer's and Parkinson's diseases, Down's syndrome, amyotropic lateral sclerosis, ischemic stroke, spinal cord injury, and Duchenne muscular dystrophy.

This text aims to fill a void between the fields of nutrition, behaviour, and cellular and molecular neurosciences by providing an integrated collection of articles that critically dissect the link between what we eat and how the brain develops and functions in health and disease. Key topics covered in depth include: caloric restriction benefit the brain and retard aging; effects of dietary antioxidants on brain function and aging; developmental and function consequences of different dietary fatty acids; and the biochemical links between dietary folic acid and psychiatric and neurodegenerative disorders.

Diet-Brain Connections fills a void between the fields of nutrition, behavior and cellular and molecular neurosciences by providing an integrated collection of articles that critically dissect the link between what we eat and how the brain develops and functions in health and disease.Key topics covered in depth include: -caloric restriction benefit the brain and retard aging; -effects of dietary antioxidants on brain function and aging; -developmental and function consequences of different dietary fatty acids; -biochemical links between dietary folic acid and psychiatric and neurodegenerative disorders; -effects of nutritional deficit during early development and behavior disorders later in life; -neurochemical basis of the benefits of widely used dietary supplements including creatine and Gingko biloba; -contribution of dietary toxins such as metals and pesticides to neurological disorders.

In Neuroprotective Signal Transduction prominent researchers and clinicians focus on how inter- and intracellular signaling mechanisms prevent the degeneration and death of neurons occurring in both acute and chronic neurodegenerative disorders. Authoritative contributions dissect the signaling pathways of an array of neuroprotective factors-ranging from neurotrophins (NGF, BDNF, NT-3, and NT-4/5), to growth factors (bFGF, IGF-1, GDNF), to cytokines (TNF, IL-1b, and TGFb), to secreted amyloid precursor proteins, to protease nexin-1. Also treated are cytoprotective signaling events that occur within injured neurons independently of intercellular signals. Neuroprotective Signal Transduction presents fundamental, cutting-edge treatment of the cellular and molecular signal transduction pathways found in human neurodegenerative conditions. The book's elucidation of the molecular cascades evolved by the nervous system to protect itself is now lead to effective strategies for preventing neuronal degeneration in such conditions as stroke, traumatic brain injury, Alzheimer's disease, Parkinson's disease, Huntington's disease, and amyotrophic lateral sclerosis, and will form the basis for powerful new drug discovery and gene therapy strategies.

This interdisciplinary review of the cellular and molecular basis of aggression shows how the nerve cell circuitry and the neurochemistry that mediates aggressive behaviors are modified by various environmental and genetic factors. The authors focus on the links to cognition and the neurotransmitter pathways that either promote or suppress violent behavior. They also examine how family environment, early life experiences, exposure to violent video games and movies, religion, and substance abuse effect violent behaviors, including participation in gangs and terrorist organizations. Various behavioral and pharmacological approaches are presented for preventing and treating personal aggression.

Cutting-edge articles review our current understanding of lipid microdomain signaling mechanisms and their physiological and pathological importance. The book describes the role of lipid rafts in learning, memory, and cancer, presents the emerging evidence that lipid rafts play critical roles in signaling pathways and the regulation of synaptic function in the nervous system, and shows how alterations in lipid raft metabolism are implicated in the pathogenesis of neurodegenerative disorders. Techniques are also described for the isolation of lipid rafts, the analysis of the lipid and protein components of lipid rafts, the imaging of lipid rafts in living cells, and the analysis of signal transduction in lipid rafts.

The term hormesis is de?ned as "a process in which exposure to a low dose of a chemical agent or environmental factor that is damaging at higher doses induces an adaptive bene?cial effect on the cell or organism" (Calabrese et al., 2007; Mattson, 2008). To survive and reproduce in harsh competitive environments, organisms and their cellular components have, through evolution, developed molecular mec- nisms to respond adaptively to various hazards or "stressors" that they encounter. Examples of such stressors include chemicals ingested in food and water (metals, phytochemicals, etc.), increased energy expenditure (running, ?ghting, cognitive challenges, etc.), and reduced energy availability (food scarcity), among others. In most cases, the response of the cell or organism to the stressor exhibits a biphasic dose response, with bene?cial/adaptive responses at low doses (improved fu- tion, increased resistance to damage and disease) and adverse/destructive effects (dysfunction, molecular damage, or even death) at high doses.The prevalence of the biphasic (hormetic) dose response characteristic of biological systems merits consideration of hormesis as a fundamental principle of biology.

In this groundbreaking book, leading experts detail the cellular and molecular cascades that cause selective degeneration of neuronal populations, and illuminate those genetic and environmental factors that are critical to the facilitation or suppression of the neuropathologic processes. Working from studies of human patients, as well as from cell culture and animal models, the authors demonstrate a heretofore unrecognized convergence of the causative pathogenetic mechanisms for clinically distinct neurological disorders. At center stage are the biochemical and molecular cascades that will ultimately lead to neuronal death-cascades involving oxyradical production, aberrant regulation of cellular ion homeostasis, activation of specific proteases, and activation of a stereotyped sequence of events involving mitochondial dysfunction. Individual chapters examine how these mechanisms-along with genetic and environmental factors-operate in Alzheimer's and Parkinson's diseases, Down's syndrome, amyotropic lateral sclerosis, ischemic stroke, spinal cord injury, and Duchenne muscular dystrophy.

This interdisciplinary review of the cellular and molecular basis of aggression shows how the nerve cell circuitry and the neurochemistry that mediates aggressive behaviors are modified by various environmental and genetic factors. The authors focus on the links to cognition and the neurotransmitter pathways that either promote or suppress violent behavior. They also examine how family environment, early life experiences, exposure to violent video games and movies, religion, and substance abuse effect violent behaviors, including participation in gangs and terrorist organizations. Various behavioral and pharmacological approaches are presented for preventing and treating personal aggression.

Techniques are also described for the isolation of lipid rafts, the analysis of the lipid and protein components of lipid rafts, the imaging of lipid rafts in living cells, and the analysis of signal transduction in lipid rafts.