Alzheimer's Disease Research Guide: Animal Models for Understanding Mechanisms and Medications

Author:   Takaomi C. Saido (Laboratory Head, RIKEN Center for Brain Science)
Publisher:   Elsevier Science Publishing Co Inc
ISBN:  

9780443289798


Pages:   300
Publication Date:   05 August 2024
Format:   Paperback
Availability:   Manufactured on demand   Availability explained
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Alzheimer's Disease Research Guide: Animal Models for Understanding Mechanisms and Medications


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Overview

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.

Full Product Details

Author:   Takaomi C. Saido (Laboratory Head, RIKEN Center for Brain Science)
Publisher:   Elsevier Science Publishing Co Inc
Imprint:   Academic Press Inc
Weight:   0.460kg
ISBN:  

9780443289798


ISBN 10:   0443289794
Pages:   300
Publication Date:   05 August 2024
Audience:   College/higher education ,  Postgraduate, Research & Scholarly
Format:   Paperback
Publisher's Status:   Active
Availability:   Manufactured on demand   Availability explained
We will order this item for you from a manufactured on demand supplier.

Table of Contents

1. Introduction: Collaboration and Competition Together to Maximize the Velocity of Research and Development 2. Pathological Chronology and Pathological Biochemistry: The Beginning of The Beginning 3. Human Genetics: Establishment of Cause-And-Effect Relationships 4. Two Major Culprits: Amyloidogenic Aß And Non-Amyloidogenic Tau 5. Exact relationship between Aß40 and Aß42 6. Metabolism of Aß: Catabolic and glimphatic systems 7. Biology of time: Temporal distance between cause and effect 8. 1st generation animal moßdels of Aß amyoloidosis: Pros and cons of overexpression paradigm 9. Creation of single APPKNOCK-IN mouse models and of single MAPTNOKCK-IN models: Demonstration of AB-Tau axis 10. Application of Mouse Models to the experimental studies of AD 11. Neuroinflammation: Microgliosis and Astrocytosis in the days of microscopic omics 12. Central and peripheral nervous system, immune systems and digestive system: AD as a systemic disorder 13. Failure of more than 400 candidate medications in clinical trials before 2020 14. Therapeutic antibodies as a Wright brothers' airplane: Clinical proof-of-concept 15. Biomarkers for presymptomatic diagnosis and prognosis 16. Targeting somatostatin receptor heterodimer for developing safe, effective and ineffective and inexpensive medications 17. Application of genome editing to the treatment of familial AD 18. Identifying significant and insignificant publications: Prelude for chapter XIX 19. Journal of negative data for the days of generative AI-assisted publication 20. Conclusions

Reviews

""Disease -modifying drugs have been approved, and the research field for Alzheimer's disease is now entering a new stage. This book is relevant during such a time of transition. This inspiring book concentrates on the essence of fighting at the frontlines of Alzheimer’s research. In particular, it conveys the importance of focusing on one's own research from a long-term perspective."" -- Kenichi Nagata, Designated Lecturer, Department of Functional Anatomy & Neuroscience, Nagoya University Graduate School of Medicine


""Disease -modifying drugs have been approved, and the research field for Alzheimer's disease is now entering a new stage. This book is relevant during such a time of transition. This inspiring book concentrates on the essence of fighting at the frontlines of Alzheimer’s research. In particular, it conveys the importance of focusing on one's own research from a long-term perspective."" -- Kenichi Nagata, Designated Lecturer, Department of Functional Anatomy & Neuroscience, Nagoya University Graduate School of Medicine ""Written by a prominent leader in the Alzheimer’s disease research field, this book is a marvelous must-read guidebook for next generations interested in Alzheimer’s disease studies, especially in animal models of Alzheimer’s disease. Each chapter is written with historical emphasis and lively manner in such a way that readers can enjoy close dialogues with the author. This is the book I looked for 8 years ago when I started Alzheimer’s disease research!"" -- Kei M Igarashi, Ph.D., Chancellor’s Fellow Associate Professor, Department of Anatomy and Neurobiology, University of California, Irvine


Author Information

Takaomi C. Saido is a graduate of Tsukuba University, Japan, where he majored in biophysics, and was subsequently trained in the Graduate School of Pharmaceutical Science, the University of Tokyo where he obtained PhD. During the graduate school years, he spent a year as a Visiting Scholar in the Department of Engineering and Applied Physics, Cornell University, NY. In the beginning of his career at the Tokyo Metropolitan Institute of Medical Science as a Research Scientist, he focused on proteolytic reactions conducted by calpain, a cytosolic calcium-activated neutral protease that modifies its substrates via limited proteolysis. His specialty was basic biochemistry, and he, for the first time in the history of proteolysis research, devised a universally applicable immunochemical method that can distinguish proteolytic products from the full-length substrates. The antibodies that created have been widely used in both basic and clinical studies worldwide (see a review, Saido et al., FASEB J, 1994). He then began collaborating with neurosurgeons and neuropathologists on brain ischemia and Alzheimer's disease (AD), respectively. The collaborations were so successful that in the 1990’s he decided to dedicate most of his time and effort to the study of the brain disorders as a Laboratory Head of RIKEN Brain Science Institute/Center for Brain Science. Although both brain ischemia (strokes) and AD cause dementia, the former had become more preventable by controlling vascular aging, whereas it has been still extremely difficult to stop the onset or to slow down the progression of AD, making him more inclined to study the latter. After discovering that amyloid b peptide (Ab) starting with pyroglutamate at positions 3 (AbN3pE) is a major species that accumulates in human brain (Saido et al., Neuron, 1995), he became interested in the catabolic mechanism of Ab. Using biochemical and reverse genetic methods, he discovered neprilysin (neutral endopeptidase) as a major in vivo Ab-degrading enzyme (Iwata et al., Nat Med, 2000; Science 2001). He hypothesized that an aging-dependent decline of neprilysin expression in the human brain may be one of the causes of sporadic AD. In the Science paper, he also predicted the possible presence of risk alleles in the MME gene encoding neprilysin, and a recent Genome-wide association study (GWAS) consistently identified two MME SNPs significantly associated with the incidence of sporadic AD (Bellenguez et al., Nat Genetics, 2022). In the course of identifying drug target(s) with specific emphasis on neprilysin, he discovered that binding of somatostatin to a somatostatin receptor heterodimer composed of subtypes 1 and 4 selectively increases neprilysin expression/activity (Saito et al., Nat Med, 2005; Saido et al. Japanese Patent 7099717, 2022), He now focuses on generating the GPCR-based medications that will be more specific/effective, safer, and more economical than immunotherapies for treating preclinical AD. His laboratory also created the world’s first single App knock-in mouse models that reconstitute AD pathology without depending on overexpression paradigm (Saito et al., Nat Neurosci, 2014); the models are being used by more than 800 groups worldwide. Consequently, he has become one of the highly cited scientists in the research community.

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