Alzheimer S Disease Lessons From Cell Biology

Like the unflinching gaze of Captain Ahab walking the deck of the Pequod, Alzheimer researchers have had their sights fixed firmly on the disease for many years. Now, as this volume amply demonstrates, accomplished researchers from other fields, who have thought deeply about cell biological problems are applying their insights to Alzheimer's disease. The contri butions here represent the text versions of the proceedings from the tenth "Colloque medecine et recherche" of the Fondation IPSEN devoted to research on Alzheimer's disease. The symposium, entitled "Alzheimer's Disease: Lessons from Cell Biology" was held in Paris on April 25, 1994. As is apparent from the varied backgrounds of the contributors, the scientific pursuit of Alzheimer's disease has begun to meld with more basic disciplines, particularly cell biology. While on the one hand, new areas of specialization are continuously emerging, the boundaries of older disciplines are increas ingly blurred. Perhaps for most of the years since the first descriptions of the disease in 1907, the science of Alzheimer's disease was descriptive, and lay in the province of pathologists. This time period, during which a great deal was learned about the topography of senile plaques and neurofibrillary tangles, culminated with an ultrastructural description of these hallmark structures. The modern era of Alzheimer's disease research opened with the iden tification of the component proteins in plaques and tangles.

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.

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 is aimed at generating an updated reservoir of scientific endeavors undertaken to unravel the complicated yet intriguing topic of neurodegeneration. Scientists from Europe, USA and India who are experts in the field of neurodegenerative diseases have contributed to this book. This book will help readers gain insight into the recent knowledge obtained from Drosophila model, in understanding the molecular mechanisms underlying neurodegenerative disorders and also unravel novel scopes for therapeutic interventions. Different methodologies available to create humanized fly models that faithfully reflects the pathogenicities associated with particular disorders have been described here. It also includes information on the exciting area of neural stem cells. A brief discussion on neurofibrillary tangles, precedes the elaborate description of lessons learnt from Drosophila about Alzheimer's, Parkinson’s, Spinomuscular Atrophy, Huntington’s diseases, RNA expansion disorders and Hereditary Spastic Paraplegia. We have concluded the book with the use of Drosophila for identifying pharmacological therapies for neurodegenerative disorders. The wide range of topics covered here will not only be relevant for beginners who are new to the concept of the extensive utility of Drosophila as a model to study human disorders; but will also be an important contribution to the scientific community, with an insight into the paradigm shift in our understanding of neurodegenerative disorders. Completed with informative tables and communicative illustrations this book will keep the readers glued and intrigued. We have comprehensively anthologized the lessons learnt on neurodegeneration from Drosophila and have thus provided an insight into the multidimensional aspects of pathogenicities of majority of the neurodegenerative disorders.

Alzheimer's disease is the most common form of dementia in the elderly; 450,000 people in the UK and 4.5 million people in the USA suffer with this disease. This 3rd edition of Neurobiology of Alzheimer's Disease gives a comprehensive and readable introduction to the disease, from molecular pathology to clinical practice. The book is intended for readers new to the field, and it also covers an extensive range of themes for those with in-depth knowledge of Alzheimer's disease. It will therefore act either as an introduction to the whole field of neurodegeneration or it will help experienced researchers to access the latest research in specialist topics. Each chapter is written by eminent scientists leading their fields in neuropathology, clinical practice and molecular neurobiology; appendices detail disease-associated proteins, their sequences, familial mutations and known structures. It will be essential reading for students interested in neurodegeneration and for researchers and clinicians, giving a coherent and cohesive approach to the whole area of research, and allowing access at different levels. For those in the pharmaceutical industry it describes the underlying molecular mechanisms involved in the pathogenesis of Alzheimer's disease and explains how current and potential therapeutics may work.

This book provides an up-to-date overview of key areas of ageing research and bridges the gap between the subcellular events and the reality of ageing as seen in clinical practice. To this end, the reader learns about the historical development and progression of clinical ageing research. All chapters address the biochemistry or cell biology of various ageing events (to the extent that the data are available) and work their way to the clinical understanding we have of ageing. The focus of this volume is on how dietary restriction, virus infection and chronic inflammation affect the ageing process. Additionally, this book discusses how phosphate metabolism and metabolic dysfunction contribute to ageing events and how various organs and tissues (e.g. tendons, ears, heart muscle, and the endocrine system) age. This book follows on from Parts I, II and III of Biochemistry and Cell Biology of Ageing within the Subcellular Biochemistry book series and aims to bring the subcellular and clinical areas into closer contact by including interesting and significant biomedical ageing topics that were not included in the earlier volumes. Comprehensive and cutting-edge, this book is a valuable resource for experienced researchers and early career scientist alike, who are interested in learning more about the fascinating and challenging question of why and how our cells age.

As indicated by its title, this monograph deals chiefly with morphologically recognizable deviations from the normal anatomical condition of the human CNS. The AD-associated pathology is illustrated from its beginnings (sometimes even in childhood) to its final form, which is reached late in life. The AD process commences much earlier than the clinically recognizable phase of the disorder, and its timeline includes an extended preclinical phase. The further the pendulum swings away from the symptomatic final stages towards the early pathology, the more obvious the lesions become, although from a standpoint of severity they are more unremarkable and thus frequently overlooked during routine neuropathological assessment. For this reason, the authors deal with the hallmark lesions in the early phases of the AD process in considerable detail