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Autophagy 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.
List of contents
Section I. Degradation mechanisms of cells
1. Degradation mechanisms of cells
Section II. Lysosomes
2. Lysosomes-neuronal degeneration in lysosomal storage disorders
Section III. The autophagic pathways
3. The autophagy pathway and its key regulators
Section IV. Amyloid beta protein and autophagy
4. Basics of amyloid beta protein in Alzheimer's disease
5. Molecular linkages among A?, tau, impaired mitophagy, and mitochondrial dysfunction in Alzheimer's disease
6. Endocytosis in ?-amyloid biology and Alzheimer's disease
Section V. Autophagy and tau protein
7. Autophagy and tau protein
8. BAG3 promotes tau clearance by regulating autophagy and other vacuolar-dependent degradative processes
9. Tau propagation and autophagy
Section VI. Autophagy and pathology in Alzheimer's disease
10. Granulovacuolar degeneration in neurodegeneration
11. Autophagy dysfunction in skeletal myopathies: Inclusion body myositis and Danon disease
Section VII. Autophagy and other disorders causing dementia
12. Autophagy in Lewy body diseases and multiple system atrophy
13. Autophagy and Huntington's disease
Section VIII. Drug discovery in Alzheimer's disease by modulating autophagy
14. Drug discovery in Alzheimer's disease by regulating autophagy
15. Drug discovery in Alzheimer's disease using metal chelators: Warning toward their uses
16. Development of autophagy enhancers for Parkinson's disease therapy
About the author
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.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.
Report
" This book edited by Professors Hamano and Mutoh covers every important aspect of the cutting-edge neurosciences of autophagy in AD and other dementing disorders, including the degradation mechanism of misfolded proteins, A degradation mechanisms by autophagy and endocytosis, degradation mechanisms of tau by autophagy, impairment of mitophagy by A and tau accumulation, propagation of tau by autophagy dysfunction, pathological feature of autophagy, autophagy disturbances in inclusion body myositis and Danon disease, and autophagy defects in other diseases causing dementia, synucleinopathy and Huntington's disease. Perspectives on novel therapeutic strategies for AD, PD, or DLB by modulating autophagy also are widely discussed. I believe this comprehensive monograph on the role of autophagy in neurodegeneration will pave the way toward deeper understanding of the pathophysiology of neurodegenerative dementia and development of novel therapeutic methods to defeat AD and other dementias." --Takeshi Iwatsubo, MD, PhD, Professor and Chair, Department of Neuropathology, Graduate School of Medicine, The University of Tokyo
