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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.
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.
ABSTRACT: Neurodegeneration describes the progressive loss of structure and function of neurons, leading ultimately to cell and organism death. Although the initiating factors of neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, and Amyotrophic Lateral Sclerosis may be different, they share common pathophysiologies. Proteinopathies, as these diseases are now termed, are characterized by atypical deposits of proteins, often due to misfolding. Associated with these deposits are dysfunctional mitochondria, oxidative stress, disrupted axonal transport, inflammation, and apoptotic cell death. If this occurs in motor neurons, as in ALS, ataxia precedes death with little or no change in cognition. On the other hand, if the deposits are found in cortical neurons, as in Alzheimer's disease, the outcome is dementia and motor function remains largely intact. Each disease is selective for particular types of neurons and brain regions. Although research has elucidated much of the molecular biology involved in these diseases, their initiating causes remain largely unknown. Most of our current understanding originated with the identification of gene mutations that cause rare familial forms of these diseases. As a result, numerous strains of transgenic animals have been developed to study neurodegenerative disease phenomena and were central to the studies presented in this body of work. Novel routes of drug and gene delivery are described here as well as characterization of the mouse models studied. In particular, this work demonstrates that the blood brain barrier is disrupted in ALS followed by the formation of autorosettes in ALS mice. In various Alzheimer's disease mouse models, it was demonstrated that the acute phase reactant alpha-1-antichymotrypsin (ACT) not only interacts with amyloid plaques, but also induces tau phosphorylation in vivo; tying together these disease hallmarks. It was also shown that small fragments of amyloid beta (1-11) could disrupt the formation of mature amyloid plaques in these mice. Lastly, it was demonstrated that mature plaques could also be decreased by intracranial delivery of granulocyte-macrophage stimulating factor (GM-CSF). My dissertation research goal was to understand and develop these treatment strategies based on protein disaggregation, neuroprotection, and inflammation, meanwhile developing novel methods for targeted delivery of molecules into the CNS of mice.
Recent Advances in Alzheimer Disease Research is a book series focusing on contemporary research on Alzheimer’s disease epidemiology, pathophysiology, diagnosis and therapy. The series features reviews by experts in neuroscience and aims to provide current information in the field to both researchers and clinicians. Down syndrome is a chromosomal disorder affecting more than 5.8 million individuals worldwide. Down syndrome can be viewed as a complex multi-system disorder as it manifests into significant physical, psychological, and cognitive abnormalities in affected persons. With aging, most adults with Down syndrome develop the clinical and neuropathological hallmarks of Alzheimer's disease. Unfortunately, no extant treatments have proven beneficial for cognitive dysfunction for either Down syndrome or Alzheimer’s disease. An incomplete understanding of the common pathogenic mechanisms that link these two disorders has limited researchers’ progress to this end. Common Pathogenic Mechanisms between Down syndrome and Alzheimer's Disease: Steps toward Therapy is a novel attempt to fill this void, by summarizing the work of world-renowned scientists in the field of Alzheimer’s disease and Down syndrome, and thus providing an unprecedented opportunity to attract attention to Down syndrome as a tool for understanding the common molecular mechanisms that underlie Alzheimer’s disease and to develop new therapies for similar neurodegenerative disorders of the brain. The book covers the fundamental pathophysiology and molecular mechanisms behind the incidence of Alzheimer’s disease in Down syndrome affected individuals as well other key topics such as diagnosis and management, in vivo brain imaging studies, and progressive neurodegeneration of the monoaminergic system. The book concludes with a review of recent clinical trials of drugs designed to mitigate cognitive dysfunction in aging adults with Down syndrome and establishes a scientific warrant for the increased testing of candidate pharmacotherapies. Common Pathogenic Mechanisms between Down syndrome and Alzheimer's Disease: Steps toward Therapy is a useful reference clinicians involved in treating Down syndrome patients as well as for neuroscience researchers seeking to understand the influence of a specific case of aneuploidy on Alzheimer’s disease incidence and its progression at the molecular level.
Animals have been used to model diseases or test new treatments since around 300 BC, and undoubtedly our ability to model disease in animals – including transgenic animals – has provided major breakthroughs in all fields of biomedical research. Due to their complexity and plurality of pathology and symptomatology, the study of neurodegenerative diseases relies heavily on animal models. These models have been developed in many species in the attempt to undercover the complex nature of the disease mechanisms involved. The ultimate goal is to test promising therapies and to manage, prevent or cure neurodegenerative disease. But because most animal models in this area do not reproduce the full phenotypical disease spectrum and the etiology and clinical presentation of neurodegenerative diseases differ from one patient to the next, the testing of these diseases in animal models often translates poorly to indices of efficacy when applied to the clinical population. Written by experts in the field with these advances and challenges in mind, this handbook provides an updated overview of the animal models being developed and used to study complex disease dynamics. The first part of the book presents an overview of animal models of various species and includes a review of new invertebrate animal models to study neurodegeneration. The second section presents the use of animal models to pinpoint disease mechanisms, and the last part of the handbook examines the various therapeutic interventions being used in models of neurodegenerative disease.
Alzheimer's Disease Research Guide: Animal Models for Understanding Mechanisms and Medications provides researchers with a comprehensive guide, detailing every aspect of Alzheimer's Disease research, including chapters on neuroinflammation, immunotherapy, biomarkers, and animal modeling. This book begins with historical perspectives of both pathological chronology and pathological biochemistry in relation to Alzheimer’s disease. Other chapters review Amyloidogenic AB and Non-Amyloidogenic tau and Metabolism of AB major components to the research and understanding of Alzheimer’s research. The book concludes with specific treatment chapters including how to develop safe, effective, and inexpensive medications and the application of genome editing to the treatment of Familial Alzheimer's Disease. Written by world renowned expert in Alzheimer’s research, this book is a valuable resource for all researchers. Reviews why familial Alzheimer’s disease is vital to understanding sporadic Alzheimer’s disease Describes the latest “game changer” animal models of Alzheimer's disease and frontotemporal dementia in detail Explains how various Alzheimer’s disease medications have failed clinical trials Discusses pros and cons of therapeutic antibodies, lecanemab and donanemab, that were recently found to be effective in recent clinical trials Details the application of genome editing as a treatment for familial Alzheimer’s disease Proposes publishing “Journal of Negative Data” for the days of generative AI-assisted publication, AI being unable to distinguish between reproducible and unreproducible data, particularly important in Alzheimer’s research
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.
As no successful therapeutic approach to treat Alzheimer's disease (AD) has been developed to date, preventative strategies and non-pharmacological interventions increasingly become a major research focus. In recent years, substantial evidence for a protective role of physical and cognitive activity on the risk of AD has been growing. In the present study, the effect of a challenging environment in combination with regular exercise on the Alzheimer-like pathology of the Tg4-42 and 5XFAD mouse models was investigated. The Tg4-42 model overexpresses N-truncated A[beta]4-42 without any mutations an ...
This manual takes a multidisciplinary approach to neurological disorders in the elderly. Comprehensive and practical, it includes the most recent diagnostic criteria and immediately accessible visual care paths including the latest pharmacologic and non-pharmacologic interventions. Covering a range of modalities, from the importance and impact of each disease to diagnostic criteria, genetics, laboratory and imaging findings, treatment and care paths, this book focuses on neurological conditions that occur commonly in older persons or which have a striking effect on their lives. The common types of dementias, Parkinson’s disease and related disorders, rapidly progressive diseases, seizure disorders and multiple sclerosis are covered. Issues commonly affecting this population, such as neurobehavioral symptoms and caregiver issues, are discussed. Neuro-Geriatrics: A Clinical Manual is aimed at any physician who treats the elderly with neurological disorders: neurologists, geriatricians and geriatric psychiatrists, both specialists and general practitioners.