Molecular Neurobiology of Alzheimer Disease and Related Disorders

1. Methods of Regulating Alzheimer Pathogenesis: Diet, Oxidative Damage and Inflammation
2. The RNA-Binding Protein Causes Aberrant Splicing of Presenilin-2 Pre-mRNA in Sporadic Alzheimer’s Disease
3. Alzheimer’s
-Secretase Mechanism Produces Amyloid- -Protein Like Peptides Simultaneously with Release of Intracellular Signaling Fragments
4. Pivotal Role of Neurofibrillary Degeneration in Alzheimer Disease and Therapeutic Targets
5. Tau Pathology of Sporadic Tauopathies
6. Deregulation of GSK-3  and JNK in a Mouse Model of Tauopathy: A Kinase Combination That Induces Alzheimer-Type Tau Hyperphosphorylation
7. Clinical Assessment of the Genetic Risk Functions in Alzheimer’s Disease
8. Hydrogen Sulfide Is Severely Decreased in Alzheimer Disease Brains
9. Functional Analysis of the Presenilin Complex and
-Secretase Activity
10. Pharmacogenomic Studies with a Combination Therapy in Alzheimer’s Disease
11. Nicotinic Receptor Stimulation Blocks Neurotoxicity Induced by Amyloid-  via the Phosphatidylinositol-3-Kinase Cascade
12. Involvement of Unfolded Protein Responses in Alzheimer’s Disease
13. Advances in the Development of Biomarkers for Alzheimer’s Disease – From CSF Total Tau and Amyloid-( 1 –42) Proteins to Phosphorylated Tau and Amyloid--Antibodies
14. Genetic Analysis of Familial Alzheimer’s Disease in a Japanese Population
15. Oxidative Stress in Alzheimer Disease: The Earliest Cytological and Biochemical Feature
16. Neurogenesis: A Promising Therapeutic Target for Alzheimer Disease and Related Disorders
17. Learning Deficits in N279K Tau Transgenic Mice and an Assembly Model of Tau Protein
18. Animal Models of Tauopathies
19. Aberrant Splicing of Tau Transcripts in Frontotemporal Dementia with Parkinsonism Linked to Chromosome 1 7
20. Tau Filament Formation and Associative Memory Deficit in Aged Mice Expressing Mutant (R406W) Human Tau
21. Activated Protein Kinases and Phosphorylated Tau Protein in Alzheimer Disease
22. A Functional Genomics Approach to the Analysis of Biological Markers in Alzheimer Disease
23. Epilogue

Alzheimer's disease affects 6-10 per cent of the elderly population, causing impairment in cognitive functions and significant disability in daily living for more than ten years. Neurofibrillary tangles, amyloid deposits and neuronal loss are the three hallmarks of Alzheimer's disease. Due to insolubility of these unique structures in Alzheimer brain tissue, they were very difficult to study by usual biochemical methods in the past. Active research is now going on to elucidate the pathogenesis of Alzheimer's disease. Major topics of neurobiological study of Alzheimer's disease include the unraveling of the molecular mechanism of neurofibrillary tangle formation in neuronal and glial cells, the molecular processing of amyloid precursor protein in intracellular organella and in extra-cellular space, and the molecular mechanism of neuronal loss.The articles in this book were selected from contributions presented by leading scientists in this field at the international symposium which took place in Osaka in 2002. This publication is essential reading for all researchers, clinicians, basic and social scientists, neurologists and psychiatrists to promote the understanding of this formidable disease.