| Description |
1 online resource (xiv, 297 pages) : illustrations (chiefly color) |
| Contents |
Cover -- Contents -- Foreword -- Preface -- Methods of Regulating Alzheimer Pathogenesis: Diet, Oxidative Damage and Inflammation -- The Amyloid Cascade in Alzheimer's Disease -- Inflammation, Oxidative Damage and Synapse Loss -- Protective Factors Reducing the Risk of Alzheimer's Disease in Epidemiological Studies -- Nonsteroidal AntiOInflammatory Drugs -- Antioxidants -- Statins -- Dietary Fish and n-3 Fatty Acids -- Testing Epidemiological Risk Factors in Animal Models -- Amyloid Cascade Interventions -- Nonsteroidal Anti-Inflammatory Drugs -- Ibuprofen and Amyloid Reduction |
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Amyloid Cascade Interventions -- Antioxidants -- Amyloid Cascade Interventions -- Mechanism of Curcumin Inhibition of Beta-Amyloidosis -- Neurodegeneration in AD vs. APPsw Mice -- Fish Oil and n-3 Fatty Acids -- Conclusions -- References -- The RNA-Binding Protein Causes Aberrant Splicing of Presenilin- 2 Pre- mRNA in Sporadic Alzheimer's Disease -- Cell Types and Stress Conditions for the Production of PS2V -- PS2V Was Detected in Sporadic Alzheimer's Disease Brains and Caused Increases in the Production of ABeta -- HMGA1a Is a PS2 Pre-mRNA-Binding Factor |
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HMGA1a Binds to a Specific Sequence of PS2 Pre-mRNA -- The Expression of HMGA a Is Induced by Hypoxic Stimuli -- HMGA1a Colocalizes with an Authentic Splicing Factor under Hypoxic Conditions -- PS2V Is Produced by the Expression of HMGA1a -- Interference of U1 snRNP Binding to 5' Splice Site by HMGA1a -- Levels of HMGA a Protein in Brains of Patients with Sporadic Alzheimer's Disease -- Conclusion -- Acknowledgements -- References -- Alzheimer's Gama-Secretase Mechanism Produces Amyloid-Beta-Protein Like Peptides Simultaneously with Release of Intracellular |
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Intramembranous Endoproteolysis Is Essential for the Novel Signaling Paradigm -- Notch-1-beta and CD44-beta Peptides, A beta -Like Fragments, Are Physiologically Secreted -- Level of an Elongated A beta-Like Peptide as a Substitute for A beta May Reflect AD-Associated Pathological Impairment of ga -- It Is Worthwhile Studying Whether Secreted N beta Peptide Level Is Upregulated in Cells of Human Malignancies -- Acknowledgement -- References -- Pivotal Role of Neurofibrillary Degeneration in Alzheimer Disease and Therapeutic Targets -- Neurofibrillary Degeneration -- Tau Kinases and Phosphatases |
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Therapeutic Targets -- Acknowledgements -- References -- Tau Pathology of Sporadic Tauopathies -- Differences of Isoform Composition of Aggregated Tau -- Differences of the Phosphorylation State of Aggregated Tau -- Differences in Proteolytic Processing of Aggregated Tau -- Conclusion -- Acknowledgement -- References -- Deregulation of GSK-3 beta and JNK in a Mouse Model of Tauopathy: A Kinase Combination That Induces Alzheimer- Type Tau Hyperphosphorylation -- Experimental Procedures -- Antibodies -- Immunoblot and Immunohistochemical Procedures |
| Summary |
Contains selected papers presented at the International Symposium on Molecular Neurobiology of Alzheimer Disease and Related Disorders held in Osaka, Japan, in October 2002 |
| Analysis |
Alzheimer's disease |
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Neurobiology |
| Bibliography |
Includes bibliographical references and index |
| Notes |
Print version record |
| Subject |
Alzheimer's disease -- Molecular aspects
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Molecular neurobiology.
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Neurobiology.
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Alzheimer Disease -- metabolism
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Alzheimer Disease -- physiopathology
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Alzheimer Disease -- genetics
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Neurobiology
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Neurobiology
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Alzheimer's disease -- Molecular aspects
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Molecular neurobiology
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Alzheimerkrankheit
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Molekularbiologie
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Neurobiologie
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Alzheimer-Krankheit -- Neurobiologie -- Molekularbiologie -- Kongress -- Osaka <2002>.
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| Genre/Form |
Konferenzschrift
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| Form |
Electronic book
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| Author |
Takeda, Masatoshi, 1949-
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Tanaka, Toshihisa, Dr.
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Cacabelos, R. (Ramón), 1955-
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S. Karger (Firm)
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| ISBN |
9783318009934 |
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3318009938 |
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