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1. Introduction
2. 'Protein conformational' brain diseases
3. Alzheimer's disease
4. Senile plaques and neurofibrillary tangles
5. Beta-amyloid (A-beta)
6. Paired helical filaments (PHFs)
7. Tau isoforms
8. Molecular genetics of AD
9. Amyloid precursor protein (APP)
10. APP processing pathways
11. APP mutations
12. Effects of APP and PS mutations
13. Amyloid aggregation
14. A-beta oligomers and mature fibrils
15. 'Amyloid cascade' hypothesis
16. A-beta toxic mechanism?
17. Butterfield (1994) and Bush (1999)
18. Does A-beta generate free radicals?
19. Spin traps
20. ESR results
21. Hydrolysis and breakdown of PBN
22. Conclusions from the spectra
23. Does A-beta generate hydrogen peroxide?
24. DMPO hydroxyl radical spectra
25. Possible mechanism of peroxide formation
26. Parkinson's disease (PD)
27. Degeneration of substantia nigra
28. Lewy bodies
29. Alpha-synuclein filaments
30. Gene mutations in familial PD
31. Alpha-synuclein and 'NAC'
32. Other amyloid peptides
33. Does alpha-synuclein generate peroxide?
34. More data on A-beta and alpha-synuclein
35. Toxic prion fragments
36. Cu(II) binding modulates PrP 106-126 toxicity
37. PrP 106-126 ESR spectra
38. Summary of PrP 106-126 data
39. Prion (PrP 121-231) ESR spectra
40. Prion (PrP 121-231) data
41. A-beta (1-40) aggregation vs. peroxide formation
42. ELISA to detect A-beta oligomers
43. Soluble A-beta oligomers generate peroxide?
44. Mature A-beta fibrils do not generate peroxide
45. Familial British dementia peptide (ABri)
46. Time course for ABri
47. Soluble ABri oligomers generate peroxide?
48. No. of CAG repeats and age of onset
49. Are intranuclear inclusions toxic?
50. Common toxic pathway?
51. Conclusions
52. References

Topics Covered

• Introduction to protein conformational brain diseases
• Alzheimer's disease, A-beta and tau
• A-beta oligomers and toxicity
• A-beta generates hydrogen peroxide
• Results from experiments using electron spin resonance spectroscopy
• Parkinson's disease
• Generation of hydrogen peroxide from alpha synuclein, toxic fragments of the prion protein and the familial British dementia peptide
• Early oligomers appear to generate hydrogen peroxide
• Huntington's disease
• Protein aggregates could be protective
• Potential common toxic pathway for these brain diseases

Links

Series:

• Protein Folding, Aggregation and Design

Categories:

• Biochemistry
• Cell Biology
• Clinical Practice
• Neuroscience

Therapeutic Areas:

• Neurology

Talk Citation

Allsop, D. (2007, October 1). Protein aggregation, metals and oxidative stress in neurodegenerative diseases [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved December 3, 2024, from https://doi.org/10.69645/EHPW4854.
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Publication History

• Published on October 1, 2007

Financial Disclosures

• Prof. David Allsop has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.