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Autophagy Dysfunction in Alzheimer's Disease and Dementia

  • Book

  • August 2022
  • Elsevier Science and Technology
  • ID: 5527338

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.

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Table 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

Authors

Tadanori Hamano 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, Japan. 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 Professor, Department of Neurology and Neuroscience, Fujita Health University Hospital, Toyoake-City, Aichi, Japan. 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.