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Few medical or scientific addresses have so unmistakeably made history as the presentation delivered by Alois Alzheimer on November 4, 1906 in Tübingen. The celebratory event "Alzheimer 100 Years and Beyond" was organized through the Alzheimer community in Germany and worldwide, in collaboration with the Fondation Ipsen. This volume, a collection of articles by the invited speakers and of a few other prominent researchers, is published as a record of those events.
This volume is arecord of the proceedings of a NATO Advanced Study institute on "Biochemical and Bio logical Markers of Neoplastic Transformation" held September 28 - October 8, 1981, at Corfu, Greece. As early as 1860, Rudolf Virchow provided the first genetic concept of cancer by postulating "Omnia ceZZuZa e ceZZuZa ejusdem generis", a modification of the then exisiting cell theory "Omnis ceZZuZa e ceZZuZa". Thus, the idea that all cells originate from the parent cell was extended to the idea that all cancer cells come from the "paren t" cancer cello But how the first cancer cell arose, or in other words, how anormal cell changed to a cancer cell, is, even after 120 years, a mystery. Exper...
Highlighting the latest and the most timely aspects of Alzheimer's disease research, this text will enable scientists in related research fields, as well as physicians working with Alzheimer's disease patients, to obtain a quick and complete overview of the current state of the art in one of the most exciting fields in neuroscience research. Leading scientists have contributed articles focusing on key developments in this field. This includes an overview about the pathology, the genetics of familial Alzheimer's disease, proteolytic generation and aggregation of amyloid -peptide, presenilins, risk factors such as ApoE, and transgenic animal models. Some of the latest developments in Alzheimer's disease research, including the effect of presenilin knock outs on amyloid -peptide generation, are also included.
Alzheimer's disease is the most common cause of senile dementia. Since the discovery in 1984 of the amyloid ?-peptide (A?) as the core protein of the senile plaques present in the brains of Alzheimer's disease sufferers, an immense amount of research has gone into mapping out the molecular basis of this debilitating disease. The aim of Alzheimer's Disease: Methods and Protocols is to bring together the main biochemical, cell biological, and molecular biological techniques and approaches that are being used to investigate the molecular basis of Alzheimer's disease. This volume begins with chapters of an introductory/ review nature. Chapter 1 provides a historical introduction to Alzheimer's d- ease with particular emphasis on the central role played by A? and its re- tion to tau. Chapter 2 examines the genetics underlying this neurodegenerative disease, covering the amyloid precursor protein, apolipoprotein E, and the presenilins. Chapter 3 presents an overview of currently available therapeutic agents and prospects for drugs of the future.
Animal models of neuro- and psychopathological states in humans are an indispensable part of both experimental neurology and biological psychiatry. Written by a team of experts, this book provides an up-to-date detailed overview of the current approaches to the design of viable animal models for eight prominent neuropsychiatric diseases. The book is specifically written with the research-oriented reader in mind — both in academia and the pharmaceutical industry. It contains first-hand information on how to design viable animal models for Alzheimer's disease, epilepsy, Huntington's disease, Parkinson's disease, addiction, depression, fear and anxiety, and schizophrenia. Each chapter also critically discusses the limitations of the animal experimental approach towards an understanding of human neuropsychiatric disorders.The book is an essential source of reference for researchers who seek to successfully continue and elaborate the experimental work that will finally lead to a better understanding of the neurobiological basis of the diseases, as well as to an improvement of both diagnosis and therapy.
This book delves into the delicate realm of neurodegenerative illnesses, navigating the vast landscape of molecular targets with care and purpose. Researchers are studying the complex pathways involved in diseases such as Alzheimer’s, Parkinson’s, and Huntington’s in order to identify specific molecules that could be targeted for therapy. The present work explores potential methods of intervention by carefully analysing neural circuits, protein misfolding, and genetic predispositions, unravelling the complexities of the human mind by focusing on individual molecular targets. As new findings emerge, reducing the severe consequences of neurodegenerative illnesses becomes increasingly possible, providing optimism for millions of people throughout the world.
This work aims to shed light on the potential causes and pathogenesis of Alzheimer's disease, Lewy body diseases and frontotemporal dementias. The focus on these clinical diseases is complemented by research reports on transgenic mouse models of alpha-synuclein, tau and amyloid accumulation in the brain. The underlying premise of the research reported in this book is that improved understanding of these protein molecules will open novel avenues of treatment and perhaps even prevention of these neurodegenerative diseases. Contributors include academic scientists, scientists in industry and clinical investigators, all committed to transferring the insights gained in basic research to the physician caring for persons with dementia.
Alzheimer's disease (AD) is the most common type of neurodegenerative disorder in the ageing population, with dementia as a common consequence. AD is defined pathologically by the appearance of extracellular senile plaques and intracellular neurofibrillary tangles, as described by Alois Alzheimer about a century ago. The causes for AD include genetic predisposition in a small population, ageing and environmental stresses in majority cases. The underlying pathogenic cascades, increases in expression of amyloid precursor protein and accumulation of Aß and reactive oxidant activity and inflammation, have the features of both adaptive, at least initially, and harmful when becoming excessive. De...