Alzheimer S Disease Pathogenesis

Alzheimer's Disease Pathogenesis: Core Concepts, Shifting Paradigms, and Therapeutic Targets, delivers the concepts embodied within its title. This exciting book presents the full array of theories about the causes of Alzheimer's, including fresh concepts that have gained ground among both professionals and the lay public. Acknowledged experts provide highly informative yet critical reviews of the factors that most likely contribute to Alzheimer's, including genetics, metabolic deficiencies, oxidative stress, and possibly environmental exposures. Evidence that Alzheimer's resembles a brain form of diabetes is discussed from different perspectives, ranging from disease mechanisms to therapeutics. This book is further energized by discussions of how neurotransmitter deficits, neuro-inflammation, and oxidative stress impair neuronal plasticity and contribute to Alzheimer's neurodegeneration. The diversity of topics presented in just the right depth will interest clinicians and researchers alike. This book inspires confidence that effective treatments could be developed based upon the expanding list of potential therapeutic targets.

Alzheimer’s disease is an increasingly common form of dementia and despite rising interest in discovery of novel treatments and investigation into aetiology, there are no currently approved treatments that directly tackle the causes of the condition. Due to its multifactorial pathogenesis, current treatments are directed against symptoms and even precise diagnosis remains difficult as the majority of cases are diagnosed symptomatically and usually confirmed only by autopsy. Alzheimer’s Disease: Recent Findings in Pathophysiology, Diagnostic and Therapeutic Modalities provides a comprehensive overview from aetiology and neurochemistry to diagnosis, evaluation and management of Alzheimer's disease, and latest therapeutic approaches. Intended to provide an introduction to all aspects of the disease and latest developments, this book is ideal for students, postgraduates and researchers in neurochemistry, neurological drug discovery and Alzheimer’s disease.

Alzheimer's Disease is an ever present problem affecting millions of people around the world and, as people's average lifespan lengthens, its prevalence is set to increase. A global effort is needed to combat the disease, including research to investigate the causes, development of effective treatments and, ultimately, prevention of the disease. Published every two years, these timely books discuss the very latest research. This new volume provides a unique source of reference to the important work being done in this field, it gives academics and clinicians an opportunity to learn about cutting edge developments and covers all aspects of Alzheimer's Disease, including diagnosis, clinical course, epidemiological course and therapeutics and disease mechanisms. Alzheimer's Disease: Advances in Etiology, Pathogenesis and Therapeutics will provide essential information for basic and clinical researchers in Alzheimer's Disease and other dementias as well as for those who care for patients.

Alzheimer’s Disease is characterized pathologically by two principal hallmark lesions: the senile plaque and the neurofibrillary tangle. Since the identification of each over 100 years ago, the major protein components have been elucidated. This has led in turn to the elaboration of metabolic cascades involving amyloid-β production in the case of the senile plaque, and phosphorylated-tau protein in the case of the neurofibrillary tangle. The pathogenesis and histogenesis of each have been the source of extensive investigation and some controversy in recent years, as both cascades have been implicated in the pathogenesis of Alzheimer’s Disease, relied upon in the diagnostic criteria for Alzheimer’s Disease at autopsy, and targeted for therapeutic intervention. With the accumulation of data and expansion of knowledge of the molecular biology of Alzheimer’s Disease, it appears that the enthusiasm for successful intervention has been premature. In this book, we detail the discovery and characterization of the major pathological lesions, their associated molecular biology, their relationship to clinical disease, and potential fundamental errors in understanding that may be leading scientific investigators in unintended directions.

Alzheimer's disease is an age-related progressive degenerative disease which constitutes the principal cause of dementia. It affects approximately 5-10% of the population over 65 years of age, rising to 20% of the population over 80 years of age. Improvements in health care in the developed world have resulted in an increasingly large elderly population and thus a growing number of Alzheimer's disease sufferers. The care of these patients presents a major and increasing human burden and drain on health care resources and thus the disease constitutes one of the major challenges to public health. Despite considerable knowledge about the clinical manifestations of Alzheimer's disease, its cause is at present unknown. This book outlines the clinical problems associated with Alzheimer's disease and seeks to provide a synthesis of knowledge of the major fields of research into the disease together with suggestions for future research. The topics covered include: neurotransmitter deficits, patterns of cerebral pathology, progression of the pathological changes, structure of neurofibrillary tangles and senile plaques, hippocampal pathology and memory impairment, animal models of amnesia and dementia, trace elements and the pathogenesis of the disease and the genetics of Alzheimer's disease. The book will be of interest to a wide variety of medical practitioners, research workers and students requiring accessible information about the current focus of research into Alzheimer's disease.

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.

This comprehensive reference provides a detailed overview of current concepts regarding the cause of Parkinson's disease-emphasizing the issues involved in the design, implementation, and analysis of epidemiological studies of parkinsonism.

The discovery that several major human neurodegenerative diseases are associated with mitochondrial dysfunction has provided new opportunities for a better understanding of these diseases. In this book, major figures in the field offer state-of-the-art reviews of the role of mitochondrial dysfunction and oxidative damage in the pathogenesis of neurodegenerative diseases. Because many of the topics presented overlap with one another, the result is the most comprehensive review of the subject to date. Mitochondria and Free Radicals in Neurodegenerative Diseases begins with a historical overview of the field presented by one of its distinguished founders. The book goes on to supply detailed information on energy metabolism in normal brain function and to explore the role of oxidative damage—which may be a consequence of mitochondrial dysfunction—in the nervous system. Other early chapters focus on energy dysfunction leading to excitotoxic cell damage, the role of mitochondrial toxins in the pathogenesis of animal models of neurodegenerative diseases, and the role of mitochondria in aging. Additional topics include: Neurologic and neuropathologic consequences of mitochondrial disorders The role of mitochondria and oxidative damage in amyotrophic lateral sclerosis, Parkinson's disease, Huntington's disease, Alzheimer's disease, and cerebellar degenerations Using MRI spectroscopy to assess energy defects in patients with neurodegenerative diseases Potential therapies for neurodegenerative diseases The role of glutamate receptor antagonists for therapy Known approaches to improving energy function in mitochondrial disorders Free radical scavengers and other innovative therapeutic approaches Cover image: Three-dimensional reconstruction of an isolated, condensed rat-liver mitochondrion, obtained by electron tomography, courtesy of Dr. Carmen A. Mannella and Wadsworth Center. Reproduced with permission from TiBS (1997) vol. 22, issue 2, pp. 37-38.