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Alzheimer disease causes the gradual deterioration of cognitive function, including severe memory loss and impairments in abstraction and reasoning. Understanding the complex changes that occur in the brain as the disease progressesincluding the accumulation of amyloid plaques and neurofibrillary tanglesis critical for the development of successful therapeutic approaches. Written and edited by leading experts in the field, this collection from Cold Spring Harbor Perspectives in Medicine includes contributions covering all aspects of Alzheimer disease, from our current molecular understanding to therapeutic agents that could be used to treat and, ultimately, prevent it. Contributors discuss the biochemistry and cell biology of amyloid -protein precursor (APP), tau, presenilin, -secretase, and apolipoprotein E and their involvement in Alzheimer disease. They also review the clinical, neuropathological, imaging, and biomarker phenotypes of the disease; genetic alterations associated with the disorder; and epidemiological insights into its causation and pathogenesis. This comprehensive volume, which includes discussions of therapeutic strategies that are currently used or under development, is a vital reference for neurobiologists, cell biologists, pathologists, and other scientists pursuing the biological basis of Alzheimer disease, as well as investigators, clinicians, and students interested in its pathogenesis, treatment, and prevention.
This book examines every major aspect of Alzheimer disease at a time when there has been no scholarly research volume on the subject published in the last 3-5 years. This edition includes expanded coverage of the cellular-level exploration of related dementing disorders, with in-depth presentation of prion diseases, Pick's disease, fronto-temporal disorders, transgenic models, and biochemistry of presenilins.
The Molecular and Cellular Basis of Neurodegenerative Diseases: Underlying Mechanisms presents the pathology, genetics, biochemistry and cell biology of the major human neurodegenerative diseases, including Alzheimer's, Parkinson's, frontotemporal dementia, ALS, Huntington's, and prion diseases. Edited and authored by internationally recognized leaders in the field, the book's chapters explore their pathogenic commonalities and differences, also including discussions of animal models and prospects for therapeutics. Diseases are presented first, with common mechanisms later. Individual chapters discuss each major neurodegenerative disease, integrating this information to offer multiple molecular and cellular mechanisms that diseases may have in common. This book provides readers with a timely update on this rapidly advancing area of investigation, presenting an invaluable resource for researchers in the field. - Covers the spectrum of neurodegenerative diseases and their complex genetic, pathological, biochemical and cellular features - Focuses on leading hypotheses regarding the biochemical and cellular dysfunctions that cause neurodegeneration - Details features, advantages and limitations of animal models, as well as prospects for therapeutic development - Authored by internationally recognized leaders in the field - Includes illustrations that help clarify and consolidate complex concepts
It is generally accepted that neuropsychiatric disorders have a biological basis. Pathological changes leading to illness have been confirmed for Alzheimer’s (amyloid plaques) and Parkinson’s disease (loss of dopaminergic transmission) and are the foundation for studies on the molecular biology of these disorders. For other neuropsychiatric disorders, in particular for schizophrenic and affective disorders, molecular causes appear to be more complex and therefore remain hypothetical, despite decades of research. Changes in a number of neuronal pathways and structures have been reported to be associated with these disorders and are currently under extensive investigation. The present volume reviews recent knowledge with emphasis on ongoing research findings. Current hypotheses based on these findings are described and discussed.
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.
As the essays in this volume show, conceptualizing dementia has always been a complex process. With contributions from noted professionals in psychiatry, neurology, molecular biology, sociology, history, ethics, and health policy, Concepts of Alzheimer Disease looks at the ways in which Alzheimer disease has been defined in various historical and cultural contexts. The book covers every major development in the field, from the first case described by Alois Alzheimer in 1907 through groundbreaking work on the genetics of the disease. Essays examine not only the prominent role that biomedical and clinical researchers have played in defining Alzheimer disease, but also the ways in which the perspectives of patients, their caregivers, and the broader public have shaped concepts.
Alzheimer's disease (AD) is the leading cause of dementia and, unfortunately, remains incurable. The social, emotional and financial implications of AD are immeasurable, and about 47 million people worldwide are affected by AD or other forms of dementia. As lifespans are improved by healthcare systems worldwide, age-associated neurodegenerative diseases are imposing an increasing challenge to science. It is becoming imperative for us to understand the causes of these diseases, AD in particular, at molecular and cellular levels. Starting with the broader picture from a biological perspective, this book takes the reader through fascinating dynamics within and outside of neurons in the brain.Alzheimer's Disease: Biology, Biophysics and Computational Models helps the reader to understand AD from mechanistic and biochemical perspectives at intra- and inter-cellular levels. It focuses on biochemical pathways and modeling associated with AD. Some of the recent research on biophysics and computational models related to AD are explained using context-driven computational and mathematical modeling and essential biology is discussed to understand the modeling research.
Alzheimer's Disease is a progressive neurodegenerative disorder of late life with devastating consequences for the afflicted and their carers and poses one of the major challenges to medical research. Until recently, little hope of effective therapies capable of slowing the disease process or preventing its occurrence was apparent. With recent advances in the genetics and molecular biology of the disease processes and the demonstration of the involvement of multiple aetiological factors, however, real chances are now appearing for the identification of preventive drugs. In this discussion, experts from disciplines ranging from molecular genetics to the clinic provide review and novel data concerning the aetiology of AD and the establishment of drugfinding screening methods.
Recent advances in genetics and brain biochemistry point to the Abeta peptide as the major culprit in causing neurodegeneration in Alzheimer’s Disease (AD). This book summarizes current knowledge of the Abeta peptide and its role in AD. Written by specialists in this fast moving area, the book covers fundamental biochemical studies on this peptide, the genetic impact on Abeta expression and processing, and various AD therapeutic strategies that target Abeta.
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.