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The subject of aluminium and Alzheimer's disease has been plagued with controversy. This controversy has served to obscure much of the scientific research in this field, and subsequently has obscured the possibility that aluminium is a contributory factor in the aetiology of Alzheimer's disease. This book brings together many of the world's leading scientists researching aluminium and life and contains their critical summaries on the known facts about aluminium toxicity in man and to offer an opinion on the implications of this knowledge on a link between aluminium and Alzheimer's disease. The subject areas of the chapters were chosen to reflect the myriad of ways that aluminium is known to impact upon mammalian physiology and function and range from clinical studies, through animal models of disease to the detailed biochemistry of aluminium toxicity. Chapters are also included on epidemiology and other factors involved in the aetiology of Alzheimer's.This is the first time that this subject has been treated in such a comprehensive manner. The research detailed in each chapter, includes the latest research in the field, it has been critically appraised and this appraisal has been used by each author to present an informed opinion of its relevance to aluminium and Alzheimer's disease. The chapters are much more than reviews; they are a statement of the state of the art and of what the future may hold for research in this field. As a whole they show the high quality of research that has been carried out in our efforts to understand the toxicity of aluminium in man and that we are far away from discounting the possibility that aluminium is a contributory factor in the aetiology of Alzheimer's disease.
This book reviews the scientific literature and the authors’ own research linking aluminum neurotoxicity with cognitive impairment and Alzheimer’s disease (AD). It focuses on aluminum levels in the brain, region-specific and subcellular distribution, and its relation to neurofibrillary tangles and amyloid beta. Further, the book stresses the importance of aluminum’s complex speciation chemistry in relation to biology, and details aluminum’s mechanism in oxidative stress and cell death, especially in connection with apoptosis and necroptosis. The electrophysiological variation and synaptic plasticity induced by aluminum are covered, while the metal’s debatable role in AD and the cross-talk between aluminum and genetic susceptibility are also discussed. In closing, the book reviews the neurotoxic effects of aluminum and its important role in the pathogenesis of AD. Given its depth of coverage, the book provides readers with a systematic summary of aluminum neurotoxicity.
To understand Alzheimer's disease (AD) is one of the major thrusts of present-day clinical research, strongly supported by more fimdamental cellular, biochemical, immunological and structural studies. It is these latter that receive attention within this book. This compilation of 20 chapters indicates the diversity of work currently in progress and summarizes the current state of knowledge. Experienced authors who are scientifically active in their fields of study have been selected as contributors to this book, in an attempt to present a reasonably complete survey of the field. Inevitably, some exciting topics for one reason or another have not been included, for which we can only apologize. Standardization of terminology is often a problem in science, not least in the Alzheimer field; editorial effort has been made to achieve standardization between the Chapters, but some minor yet acceptable personal / author variation is still present, i. e. P-amyloid/amyloid-P; Ap42/Apl-42/APi. 42! The book commences with a broad survey of the contribution that the range of available microscopical techniques has made to the study of Alzheimer's amyloid plaques and amyloid fibrillogenesis. This chapter also serves as an Introduction to the book, since several of the topics introduced here are expanded upon in later chapters. Also, it is significant to the presence of this chapter that the initial discovery of brain plaques, by Alois Alzheimer, utilized light microscopy, a technique that continues to be extremely valuable in present-day AD research.
The brain is the most complex organ in our body. Indeed, it is perhaps the most complex structure we have ever encountered in nature. Both structurally and functionally, there are many peculiarities that differentiate the brain from all other organs. The brain is our connection to the world around us and by governing nervous system and higher function, any disturbance induces severe neurological and psychiatric disorders that can have a devastating effect on quality of life. Our understanding of the physiology and biochemistry of the brain has improved dramatically in the last two decades. In particular, the critical role of cations, including magnesium, has become evident, even if incompletely understood at a mechanistic level. The exact role and regulation of magnesium, in particular, remains elusive, largely because intracellular levels are so difficult to routinely quantify. Nonetheless, the importance of magnesium to normal central nervous system activity is self-evident given the complicated homeostatic mechanisms that maintain the concentration of this cation within strict limits essential for normal physiology and metabolism. There is also considerable accumulating evidence to suggest alterations to some brain functions in both normal and pathological conditions may be linked to alterations in local magnesium concentration. This book, containing chapters written by some of the foremost experts in the field of magnesium research, brings together the latest in experimental and clinical magnesium research as it relates to the central nervous system. It offers a complete and updated view of magnesiums involvement in central nervous system function and in so doing, brings together two main pillars of contemporary neuroscience research, namely providing an explanation for the molecular mechanisms involved in brain function, and emphasizing the connections between the molecular changes and behavior. It is the untiring efforts of those magnesium researchers who have dedicated their lives to unraveling the mysteries of magnesiums role in biological systems that has inspired the collation of this volume of work.
Understanding the impact of diet, exercise, genetics, and hormones on the risk and development of Alzheimer’s and other neurogenerative diseases Diet is widely known to impact on neurological function. Nevertheless, academic texts discussing this relationship are relatively few in number. This book therefore fills an important gap in the current literature. Opening with an overview of neurodegenerative diseases, particularly Alzheimer’s disease, the text then focuses on explaining the means by which glycemic control and lipid metabolism – and associated nutritional and lifestyle variables – may factor into such disorders’ prevention and treatment. An international group of experts in the fields of food science and neurodegeneration have contributed chapters that examine Alzheimer’s disease within a broad range of contexts. Offering dietary, genetic, and hormonal perspectives, the authors explore topics ranging from sugar consumption to digestive fermentation, and Alzheimer’s disease animal models to the cognition-enhancing effects of physical exercise. Also included are overviews of the latest research into current and developing methods of treatment and diagnosis, as well as differential diagnostics. This groundbreaking book: Explores how glucose metabolism, insulin resistance, lipid metabolism, and high intake of refined carbohydrates are linked to Alzheimer's disease Discusses how genetic makeup can impact risk of Alzheimer’s and Parkinson’s disease Examines cognitive changes in neurodegeneration, lists current tests for determining cognitive impairment, and provides information concerning differential diagnosis Discusses potential advantages of increasing antioxidant and micronutrient intake Reviews hormonal influences on neurodegeneration Examines the links between protein intake and Alzheimer’s disease. Neurodegeneration and Alzheimer's Disease is an essential resource for researchers, medical practitioners, dietitians, and students with an interest in neurological diseases and their diagnosis and risk factors, as well as diet-related conditions such as diabetes and obesity. Lifestyle and diet influence neurodegeneration risk, and a better understanding of this evidence amongst health professionals will hopefully lead to greater public awareness of how to reduce the likelihood of these widespread conditions.
Phytochemicals are naturally occurring bioactive compounds found in edible fruits, plants, vegetables, and herbs. Unlike vitamins and minerals, phytochemicals are not needed for the maintenance of cell viability, but they play a vital role in protecting neural cells from inflammation and oxidative stress associated with normal aging and acute and chronic age-related brain diseases. Neuroprotective Effects of Phytochemicals in Neurological Disorders explores the advances in our understanding of the potential neuroprotective benefits that these naturally occurring chemicals contain. Neuroprotective Effects of Phytochemicals in Neurological Disorders explores the role that a number of plant-based chemical compounds play in a wide variety of neurological disorders. Chapters explore the impact of phytochemicals on neurotraumatic disorders, such as stroke and spinal cord injury, alongside neurodegenerative diseases such as Alzheimer's and Parkinson's Disease, as well as neuropsychiatric disorders such as depression and schizophrenia. The chapters and sections of this book provide the reader with a big picture view of this field of research. Neuroprotective Effects of Phytochemicals in Neurological Disorders aims to present readers with a comprehensive and cutting edge look at the effects of phytochemicals on the brain and neurological disorders in a manner useful to researchers, neuroscientists, clinical nutritionists, and physicians.
A primary care doctor is skeptical of his patient’s concerns. A hospital nurse or intern is unaware of a drug’s potential side effects. A physician makes the most “common” diagnosis while overlooking the signs of a rarer and more serious illness, and the patient doesn’t see the necessary specialist until it’s too late. A pharmacist dispenses the wrong drug and a patient dies as a result. Sadly, these kinds of mistakes happen all the time. Each year, 6.1 million Americans are harmed by diagnostic mistakes, drug disasters, and medical treatments. A decade ago, the Institute of Medicine estimated that up to 98,000 people died in hospitals each year from preventable medical errors. And new research from the University of Utah, HealthGrades of Denver, and elsewhere suggests the toll is much higher. Patient advocates and bestselling authors Joe and Teresa Graedon came face-to-face with the tragic consequences of doctors’ screwups when Joe’s mother died in Duke Hospital—one of the best in the world—due to a disastrous series of entirely preventable errors. In Top Screwups Doctors Make and How to Avoid Them, the Graedons expose the most common medical mistakes, from doctor’s offices and hospitals to the pharmacy counters and nursing homes. Patients across the country shared their riveting horror stories, and doctors recounted the disastrous—and sometimes deadly—consequences of their colleagues’ oversights and errors. While many patients feel vulnerable and dependent on their health care providers, this book is a startling wake-up call to how wrong doctors can be. The good news is that we can protect ourselves, and our loved ones, by being educated and vigilant medical consumers. The Graedons give patients the specific, practical steps they need to take to ensure their safety: the questions to ask a specialist before getting a final diagnosis, tips for promoting good communication with your doctor, presurgery checklists, how to avoid deadly drug interactions, and much more. Whether you’re sick or healthy, young or old, a parent of a young child, or caring for an elderly loved one, Top Screwups Doctors Make and How to Avoid Them is an eye-opening look at the medical mistakes that can truly affect any of us—and an empowering guide that explains what we can do about it.
The instant New York Times and Wall Street Journal bestseller A groundbreaking plan to prevent and reverse Alzheimer’s Disease that fundamentally changes how we understand cognitive decline. Everyone knows someone who has survived cancer, but until now no one knows anyone who has survived Alzheimer's Disease. In this paradigm shifting book, Dale Bredesen, MD, offers real hope to anyone looking to prevent and even reverse Alzheimer's Disease and cognitive decline. Revealing that AD is not one condition, as it is currently treated, but three, The End of Alzheimer’s outlines 36 metabolic factors (micronutrients, hormone levels, sleep) that can trigger "downsizing" in the brain. The protocol shows us how to rebalance these factors using lifestyle modifications like taking B12, eliminating gluten, or improving oral hygiene. The results are impressive. Of the first ten patients on the protocol, nine displayed significant improvement with 3-6 months; since then the protocol has yielded similar results with hundreds more. Now, The End of Alzheimer’s brings new hope to a broad audience of patients, caregivers, physicians, and treatment centers with a fascinating look inside the science and a complete step-by-step plan that fundamentally changes how we treat and even think about AD.
Features that characterize the aging process include the gradual accumulation of cell damage after prolonged exposure to oxidative and inflammatory events over a lifetime. In addition to the accretion of lesions, the intrinsic levels of pro-oxidant and aberrant immune responses are elevated with age. These adverse events are often further enhanced by the chronic and slow progressing diseases that characterize the senescent brain and cardiovascular system. The incidence of some disorders such as Alzheimer's disease and vascular diseases are sufficiently prevalent in the extreme elderly that these disorders can arguably be considered "normal". Aging and Aging-Related Disorders examines the interface between normal and pathological aging, and illustrates how this border can sometimes be diffuse. It explores and illustrates the processes underlying the means by which aging becomes increasingly associated with inappropriate levels of free radical activity and how this can serve as a platform for the progression of age-related diseases. The book provides chapters that examine the interactive relationship between systems in the body that can enhance or sometimes even limit cellular longevity. In addition, specific redox mechanisms in cells are discussed. Another important aspect for aging discussed here is the close relationship between the systems of the body and exposure to environmental influences of oxidative stress that can affect both cellular senescence and a cell’s nuclear DNA. What may be even more interesting to note is that these external stressors are not simply confined to illnesses usually associated with aging, but can be evident in maturing and young individuals. A broad range of internationally recognized experts have contributed to this book. Their aim is to successfully highlight emerging knowledge and therapy for the understanding of the basis and development of aging–related disorders.
Due to that at present, the majority of diseases are associated with alterations in oxidative stress and inflammatory processes, and in that Nrf-2 is a modulator of these processes; knowing how this transcriptional factor functions and is regulated opens a therapeutic window to diverse diseases. Therefore, the efforts of various investigation groups are centered on finding activators and/or inhibitors of Nrf-2 to prevent or control diverse diseases, for example, cancer, where it would be important to regulate Nrf-2 in order for it to activate apoptosis pathways in cancerogenous cells, or in neurodegenerative diseases where cell death is predominant, it would be important for Nrf-2 to activate antiapoptotic pathways.