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Autophagy Dysfunction in Alzheimer's Disease and Dementia
- 1st Edition - August 20, 2022
- Editors: Tadanori Hamano, Tatsuro Mutoh
- Language: English
- Paperback ISBN:9 7 8 - 0 - 3 2 3 - 8 9 9 0 6 - 2
- eBook ISBN:9 7 8 - 0 - 3 2 3 - 8 9 9 1 4 - 7
Autophagy Dysfunction in Alzheimer’s Disease and Dementia provides an overview for researchers and clinicians on the mechanisms involved in protein degradation in Alzhei… Read more
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Request a sales quoteAutophagy Dysfunction in Alzheimer’s Disease and Dementia provides an overview for researchers and clinicians on the mechanisms involved in protein degradation in Alzheimer’s. The book discusses the implication of autophagy dysfunction in these diseases and how it causes degenerated proteins, including aggregated tau and aggregated amyloid protein. Other sections explores the possibilities of potential drug development through autophagy modulation, making this a great resource on the study of how autophagy dysfunction has been linked to the accumulation of misfolded proteins that cause death of neurons in Alzheimer’s and other neurodegenerative diseases.
- Discusses the implication of autophagy dysfunction in neurodegenerative diseases
- Highlights the mechanisms involved in protein degradation
- Explores the possibilities of drug development through autophagy modulation
Neuroscientists, neurologists, psychiatrists and geriatricians. Advanced graduate students
- Cover image
- Title page
- Table of Contents
- Copyright
- Dedication
- Contributors
- Foreword
- Preface
- Acknowledgments
- Section I: Degradation mechanisms of cells
- Chapter 1: Degradation mechanisms of cells
- Abstract
- 1: Neurons are highly polarized cells with the sophisticated trafficking system
- 2: Ubiquitin-proteasome system: UPS
- 3: Autophagy-endolysosomal system: APELS
- 4: Integration of cellular degradation systems
- References
- Section II: Lysosomes
- Chapter 2: Lysosomes-neuronal degeneration in lysosomal storage disorders
- Abstract
- 1: Lysosomes
- 2: Lysosomal storage diseases
- 3: Impairment of lysosomal activity and alteration in the sphingolipid composition of cell membranes: A possible link with the onset of neuronal damage in LSD
- 4: Involvement of mitochondrial impairment in the onset of neurodegeneration in lysosomal storage diseases
- 5: Involvement of lysosomal impairment in the neuroinflammation
- References
- Section III: The autophagic pathways
- Chapter 3: The autophagy pathway and its key regulators
- Abstract
- Acknowledgment
- 1: The autophagy machinery
- 2: Key regulators and signaling pathways of autophagy
- 3: Selective autophagy regulated by autophagic receptors
- 4: Concluding remarks
- References
- Section IV: Amyloid beta protein and autophagy
- Chapter 4: Basics of amyloid β-protein in Alzheimer’s disease
- Abstract
- 1: What is amyloid β?
- 2: Production and formation
- 3: Aggregation
- 4: Regulation of Aβ concentration in the brain
- 5: Decomposition and excretion
- 6: Relationship between Aβ and disease (including gene mutation)
- 7: Intervention strategy
- References
- Chapter 5: Molecular linkages among Aβ, tau, impaired mitophagy, and mitochondrial dysfunction in Alzheimer’s disease
- Abstract
- 1: Introduction
- 2: Mitochondrial dysfunction
- 3: Defective mitophagy in AD
- 4: Mitochondrial dysfunction and defective mitophagy at the circuit and behavioral level
- 5: Future research
- References
- Chapter 6: Endocytosis in β-amyloid biology and Alzheimer’s disease
- Abstract
- 1: Introduction
- 2: The flavors of endocytosis in the brain
- 3: The MO(F) of Aβ
- 4: Endocytosis in a phagocytic world
- 5: Adding a modifier, a new world for endocytosis in the AD brain
- 6: Endocytosis in a starry world
- 7: Exploiting endocytosis for therapeutic gain
- 8: Recycling full circle, a summary
- References
- Section V: Autophagy and tau protein
- Chapter 7: Autophagy and tau protein
- Abstract
- Acknowledgments
- 1: Introduction
- 2: Tau protein
- 3: Autophagy
- 4: Disturbance of the autophagy-lysosome system in AD and related disorders
- 5: Tau degradation pathway
- 6: Mitophagy and tau
- 7: Diabetes, tau, and autophagy
- 8: Propagation of tau by the disruption of autophagy
- 9: Potential of autophagy modulators as a treatment for AD
- 10: Conclusion
- References
- Chapter 8: BAG3 promotes tau clearance by regulating autophagy and other vacuolar-dependent degradative processes
- Abstract
- Acknowledgments
- 1: Introduction
- 2: BAG3 protein
- 3: Summary
- References
- Chapter 9: Tau propagation and autophagy
- Abstract
- 1: Introduction
- 2: Tau propagation mechanisms
- 3: Autophagic impairment promotes Tau aggregation
- 4: Pharmacological agents modulating Tau propagation
- 5: Conclusion
- References
- Section VI: Autophagy and pathology in Alzheimer’s disease
- Chapter 10: Granulovacuolar degeneration in neurodegeneration
- Abstract
- Acknowledgment
- 1: Introduction
- 2: Neuropathological features of granulovacuolar degeneration (GVD) in neurons
- 3: What kind of organelle are GVBs?
- 4: GVB-like structures in oligodendroglia in multiple system atrophy
- References
- Chapter 11: Autophagy dysfunction in skeletal myopathies: Inclusion body myositis and Danon disease
- Abstract
- 1: Autophagy and autophagic vacuoles
- 2: Autophagic vacuolar myopathy
- 3: Inclusion body myositis
- 4: Danon disease
- 5: Conclusion
- References
- Section VII: Autophagy and other disorders causing dementia
- Chapter 12: Autophagy in Lewy body diseases and multiple system atrophy
- Abstract
- Acknowledgments
- 1: Introduction
- 2: Autophagy
- 3: Lewy body diseases
- 4: MSA
- 5: Conclusions
- References
- Chapter 13: Autophagy and Huntington’s disease
- Abstract
- 1: Introduction
- 2: Macroautophagy in HD
- 3: Physiological function of Htt in autophagy
- 4: Autophagy: A therapeutic target
- 5: Conclusion
- References
- Section VIII: Drug discovery in Alzheimer’s disease by modulating autophagy
- Chapter 14: Drug discovery in Alzheimer’s disease by regulating autophagy
- Abstract
- 1: Introduction
- 2: Drugs that induce autophagy
- 3: Caspase activation and autophagy
- 4: Conclusion
- References
- Chapter 15: Drug discovery in Alzheimer’s disease using metal chelators: Warning toward their usage
- Abstract
- 1: Introduction
- 2: Abnormal metals in AD patients
- 3: Clioquinol and SMON (subacute myelo-optico-neuropathy)
- 4: Conclusion
- References
- Chapter 16: Development of autophagy enhancers for Parkinson’s disease therapy
- Abstract
- Acknowledgment
- 1: Features of Parkinson’s disease
- 2: Current PD therapy
- 3: α-Synuclein accumulation in PD
- 4: Autophagy impairment in PD
- 5: Targeting macroautophagy for potential PD therapy
- 6: Targeting lysosome for potential PD therapy
- 7: Conclusions and future perspectives
- References
- Index
- No. of pages: 356
- Language: English
- Edition: 1
- Published: August 20, 2022
- Imprint: Academic Press
- Paperback ISBN: 9780323899062
- eBook ISBN: 9780323899147
TH
Tadanori Hamano
Dr. Tadanori Hamano is a Clinical Professor in the Department of Neurology at University of Fukui Hospital. He’s also an Associate Professor, on the Second Department of Internal Medicine, Faculty of Medical Sciences at University of Fukui. His clinical service focuses on patients with diseases involving the central and peripheral nervous system. His research is focused on autophagic activation in the treatment of Alzheimer’s disease.
Affiliations and expertise
Clinical Professor, Department of Neurology, University of Fukui Hospital, Fukui, Japan; Associate Professor, Second Department of Internal Medicine, Faculty of Medical Sciences, University of Fukui, Fukui, JapanTM
Tatsuro Mutoh
Tatsuro Mutoh, MD, PhD got his MD and PhD degree from Nagoya University School of Medicine, Japan in 1980 and 1986, respectively. He was appointed as assistant Prof. at Fukui Medical School in 1986. Then, he moved to National Institutes of Health (NIH), NICHD, USA as a visiting fellow from 1987-1990, where he purified novel nerve growth factor-responsive protein kinases and was engaged in the analyses of signal transduction of neurotrophic factors in neuronal cells. He was promoted to full professor and Chairman at Department of Neurology, Fujita Health University School of Medicine, Japan in 2006 and was ordered to serve concurrently to Fujita Health University Chubu International Airport Medical Clinic as a Director and Prof. in 2020. His expertise is neuroglycobiology of neurodegenerative disorders, protein-lipid interaction, and neuroimmunology. He has been acting as board member of Front Cell Neurosci, Front In Biosci and so on.
Affiliations and expertise
Professor, Department of Neurology and Neuroscience, Fujita Health University Hospital, Toyoake-City, Aichi, JapanRead Autophagy Dysfunction in Alzheimer's Disease and Dementia on ScienceDirect