Protein Aggregation and Fibrillogenesis in Cerebral and Systemic Amyloid Disease
Herausgegeben:Harris, J. Robin
Protein Aggregation and Fibrillogenesis in Cerebral and Systemic Amyloid Disease
Herausgegeben:Harris, J. Robin
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This volume of the Subcellular Biochemistry series is the result of the long-standing research interest of the editor in the molecular mechanism underlying Alzheimer's disease and other amyloid diseases, indicated also by the earlier book in the series (Volume 38), devoted to Alzheimer's disease. The broad coverage within the present amyloidogenesis book represents an attempt to collate current knowledge relating to the proteins and peptides involved in most of the known amyloid diseases, together with some amyloid/fibril-forming proteins and peptides that are not involved in diseases. Thus,…mehr
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This volume of the Subcellular Biochemistry series is the result of the long-standing research interest of the editor in the molecular mechanism underlying Alzheimer's disease and other amyloid diseases, indicated also by the earlier book in the series (Volume 38), devoted to Alzheimer's disease. The broad coverage within the present amyloidogenesis book represents an attempt to collate current knowledge relating to the proteins and peptides involved in most of the known amyloid diseases, together with some amyloid/fibril-forming proteins and peptides that are not involved in diseases. Thus, the range of topics included is comprehensive and furthermore it was thought appropriate to include both basic science and clinical presentation of the subjects under discussion.
Produktdetails
- Produktdetails
- Subcellular Biochemistry 65
- Verlag: Springer / Springer Netherlands
- Artikelnr. des Verlages: 978-94-007-5415-7
- 2012
- Seitenzahl: 668
- Erscheinungstermin: 6. Dezember 2012
- Englisch
- Abmessung: 241mm x 160mm x 41mm
- Gewicht: 1220g
- ISBN-13: 9789400754157
- ISBN-10: 9400754159
- Artikelnr.: 36064983
- Subcellular Biochemistry 65
- Verlag: Springer / Springer Netherlands
- Artikelnr. des Verlages: 978-94-007-5415-7
- 2012
- Seitenzahl: 668
- Erscheinungstermin: 6. Dezember 2012
- Englisch
- Abmessung: 241mm x 160mm x 41mm
- Gewicht: 1220g
- ISBN-13: 9789400754157
- ISBN-10: 9400754159
- Artikelnr.: 36064983
1. Introduction and Technical Survey. - 2. Fibril Formation by Short Synthetic Peptides. - 3. In vitro Oligomerization and Fibrillogenesis of Amyloid-beta Peptides. - 4. Tau Fibrillogenesis. - 5. Prion protein Aggregation and Fibrillogenesis In vitro. - 6. -Synuclein Aggregation and Modulating Factors. - 7. Pathological Self-aggregation of beta2-microglobulin: A Challenge for Protein Biophysics. - 8. Islet amyloid polypeptide - Aggregation and fibrillogenesis in vitro and its Inhibition. - 9. Mechanisms of Transthyretin Aggregation and Toxicity. - 10. Fibrillogenesis of Huntingtin and Other Glutamine Containing Proteins. - 11. Aggregation and Fibrillogenesis of Proteins not Associated with Disease - A few Case Studies. - 12. Experimental Inhibition of Peptide Fibrillogenesis by Synthetic Peptides, Carbohydrates and Drugs. - 13. Experimental inhibition of fibrillogenesis and neurotoxicity by amyloid-beta (Abeta) and other disease-related peptides/proteins by plant extracts and herbal compounds. - 14. Alzheimer's Disease. - 15. Modeling the Polyglutamine Aggregation Pathway in Huntington's Disease: from Basic Studies to Clinical Applications. - 16. Parkinson's Disease. - 17. Human Prion Diseases: From Kuru to Variant Creutzfeldt-Jakob Diseasae. - 18. Animal Prion Diseases. - 19. beta2-microglobulin Amyloidosis. - 20. Systemic AA Amyloidosis. - 21. Familial Amyloidotic Polyneuropathy and Transthyretin. - 22. The Challenge of Systemic Immunoglobulin Light-chain Amyloidosis (AL).
1. Introduction and Technical Survey. - 2. Fibril Formation by Short Synthetic Peptides. - 3. In vitro Oligomerization and Fibrillogenesis of Amyloid-beta Peptides. - 4. Tau Fibrillogenesis. - 5. Prion protein Aggregation and Fibrillogenesis In vitro. - 6. α-Synuclein Aggregation and Modulating Factors. - 7. Pathological Self-aggregation of β2-microglobulin: A Challenge for Protein Biophysics. - 8. Islet amyloid polypeptide – Aggregation and fibrillogenesis in vitro and its Inhibition. - 9. Mechanisms of Transthyretin Aggregation and Toxicity. - 10. Fibrillogenesis of Huntingtin and Other Glutamine Containing Proteins. - 11. Aggregation and Fibrillogenesis of Proteins not Associated with Disease – A few Case Studies. - 12. Experimental Inhibition of Peptide Fibrillogenesis by Synthetic Peptides, Carbohydrates and Drugs. - 13. Experimental inhibition of fibrillogenesis and neurotoxicity by amyloid-beta (Aβ) and other disease-related peptides/proteins by plant extracts and herbal compounds. - 14. Alzheimer’s Disease. - 15. Modeling the Polyglutamine Aggregation Pathway in Huntington’s Disease: from Basic Studies to Clinical Applications. - 16. Parkinson’s Disease. - 17. Human Prion Diseases: From Kuru to Variant Creutzfeldt-Jakob Diseasae. - 18. Animal Prion Diseases. - 19. β2-microglobulin Amyloidosis. - 20. Systemic AA Amyloidosis. - 21. Familial Amyloidotic Polyneuropathy and Transthyretin. - 22. The Challenge of Systemic Immunoglobulin Light-chain Amyloidosis (AL).
1. Introduction and Technical Survey. - 2. Fibril Formation by Short Synthetic Peptides. - 3. In vitro Oligomerization and Fibrillogenesis of Amyloid-beta Peptides. - 4. Tau Fibrillogenesis. - 5. Prion protein Aggregation and Fibrillogenesis In vitro. - 6. -Synuclein Aggregation and Modulating Factors. - 7. Pathological Self-aggregation of beta2-microglobulin: A Challenge for Protein Biophysics. - 8. Islet amyloid polypeptide - Aggregation and fibrillogenesis in vitro and its Inhibition. - 9. Mechanisms of Transthyretin Aggregation and Toxicity. - 10. Fibrillogenesis of Huntingtin and Other Glutamine Containing Proteins. - 11. Aggregation and Fibrillogenesis of Proteins not Associated with Disease - A few Case Studies. - 12. Experimental Inhibition of Peptide Fibrillogenesis by Synthetic Peptides, Carbohydrates and Drugs. - 13. Experimental inhibition of fibrillogenesis and neurotoxicity by amyloid-beta (Abeta) and other disease-related peptides/proteins by plant extracts and herbal compounds. - 14. Alzheimer's Disease. - 15. Modeling the Polyglutamine Aggregation Pathway in Huntington's Disease: from Basic Studies to Clinical Applications. - 16. Parkinson's Disease. - 17. Human Prion Diseases: From Kuru to Variant Creutzfeldt-Jakob Diseasae. - 18. Animal Prion Diseases. - 19. beta2-microglobulin Amyloidosis. - 20. Systemic AA Amyloidosis. - 21. Familial Amyloidotic Polyneuropathy and Transthyretin. - 22. The Challenge of Systemic Immunoglobulin Light-chain Amyloidosis (AL).
1. Introduction and Technical Survey. - 2. Fibril Formation by Short Synthetic Peptides. - 3. In vitro Oligomerization and Fibrillogenesis of Amyloid-beta Peptides. - 4. Tau Fibrillogenesis. - 5. Prion protein Aggregation and Fibrillogenesis In vitro. - 6. α-Synuclein Aggregation and Modulating Factors. - 7. Pathological Self-aggregation of β2-microglobulin: A Challenge for Protein Biophysics. - 8. Islet amyloid polypeptide – Aggregation and fibrillogenesis in vitro and its Inhibition. - 9. Mechanisms of Transthyretin Aggregation and Toxicity. - 10. Fibrillogenesis of Huntingtin and Other Glutamine Containing Proteins. - 11. Aggregation and Fibrillogenesis of Proteins not Associated with Disease – A few Case Studies. - 12. Experimental Inhibition of Peptide Fibrillogenesis by Synthetic Peptides, Carbohydrates and Drugs. - 13. Experimental inhibition of fibrillogenesis and neurotoxicity by amyloid-beta (Aβ) and other disease-related peptides/proteins by plant extracts and herbal compounds. - 14. Alzheimer’s Disease. - 15. Modeling the Polyglutamine Aggregation Pathway in Huntington’s Disease: from Basic Studies to Clinical Applications. - 16. Parkinson’s Disease. - 17. Human Prion Diseases: From Kuru to Variant Creutzfeldt-Jakob Diseasae. - 18. Animal Prion Diseases. - 19. β2-microglobulin Amyloidosis. - 20. Systemic AA Amyloidosis. - 21. Familial Amyloidotic Polyneuropathy and Transthyretin. - 22. The Challenge of Systemic Immunoglobulin Light-chain Amyloidosis (AL).