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1. Introduction
2. Free radical oxidative stress
3. Brain is poised for oxidative damage
4. Radicals formation can lead to proteins damage
5. Protein oxidation: assessed by protein carbonyls
6. Lipid peroxidation
7. Formation of 3-nitrotyrosine (1)
8. Formation of 3-nitrotyrosine (2)
9. Alzheimer's disease (AD)
10. Characteristics of Alzheimer's disease
11. Aging - the biggest risk factor for AD
12. Slice of an AD brain
13. Senile plaques
14. From amyloid-precursor-protein to amyloid-beta
15. Amyloid-beta peptide
16. Abeta(1-42) is central to the pathogenesis of AD
17. AD brain is under oxidative stress
18. Model for AD pathogenesis
19. ROS production by Abeta(1-42)
20. Abeta (1-42) causes neuronal protein oxidation
21. Abeta(1-42) causes loss of CK and GS activities
22. Abeta(1-42)-induced lipid peroxidation
23. Abeta(1-42) causes HNE formation
24. Michael addition process
25. HNE formation can lead to proteins damage
26. Modification of ion-motive ATPases by HNE
27. Modification of GLT-1 by HNE
28. Glutamate-induced excitotoxicity
29. HNE and acrolein
30. Detoxification involving MRP-1
31. GST and MRP-1 are oxidatively modified by HNE
32. Prediction
33. Abeta(1-42) addition leads to Ca accumulation
34. What is the mechanism of calcium accumulation?
35. Methionine is key to Abeta(1-42)-induced effect
36. Results of mutation in Met35 of Abeta(1-42)
37. Protein oxidation in transgenic C. elegans
38. Formation of sulfuramyl free radical
39. Met radical-induced protein/lipid oxidation
40. Importance of Abeta(1-42) secondary structure
41. Results of disrupting the secondary structure (1)
42. Results of disrupting the secondary structure (2)
43. Sulfuranyl free radical in Abeta peptides
44. Loss of oxidative toxicity of Abeta (1-42)
45. Hypothesis
46. Human Abeta(1-42) expressed in C.elegans
47. Assessment of protein oxidation using the model
48. Amyloid deposits using X-34
49. Abeta toxicity and aggregates of the peptide
50. Oxidative stress in mild cognitive impairment brain
51. Oxidative stress is an early event in AD
52. Lipid peroxidation in MCI brain
53. 3-NT levels in MCI brain
54. Location of senile pluqes in an AD brain
55. Redox proteomics
56. Proteomics and disease
57. Book about redox proteomics
58. First use of proteomics in AD
59. Proteomics and oxidative modifications in AD
60. 2-dimensional gel electrophoresis
61. Identification of oxidatively modified proteins (1)
62. Identification of oxidatively modified proteins (2)
63. MS analysis and probability plots of three proteins
64. Proteins identified in Butterfield laboratory
65. Classification of the identified proteins by function
66. Oxidatively modified PIN-1 in AD brain
67. PIN-1 and AD
68. PIN-1 structure
69. Redox proteomics of MCI brain
70. Oxidatively modified proteins in MCI hippocampus
71. Elevated levels of cell cycle proteins in MCI brain
72. Proteins important in conversion from MCI to AD
73. Recapitulation of the identified proteins
74. Identification of oxidized proteins in vivo
75. Groups of proteins identified by proteomics
76. Protein oxidation and Abeta(1-42) expression
77. The C.elegans Abeta(1-42) proteomics study
78. Proteomics analysis of brain in canine model
79. Why the canine model?
80. Diet treatment
81. Behavioral enrichment
82. Hypothesis of the aging Beagle study
83. Decreased protein oxidation in aged Beagles
84. Increased antioxidant enzyme activity after EA
85. EA increased expression of neuroprotective HO-1
86. Cu, Zn-SOD and GAPDH expression
87. Identification of oxidized proteins in aged Beagles
88. Summary of the Beagle study results
89. Implications for reducing risk for AD development
90. Cellular processes leading to neurodegeneration
91. Redox proteomics analysis - other disorders
92. Summary: Abeta(1-42) induction
93. Summary: Abeta(1-42) and oxidative stress
94. Summary: Abeta(1-42) forms reactive alkenals
95. Summary: Abeta(1-42) excitotoxic mechanisms
96. Summary: proteomics
97. Summary: modified proteins
98. Summary: Abeta peptide-oxidative stress model
99. Recapitulation of the AD pathogenesis model
100. Acknowledgements

Topics Covered

• Alzheimer's disease and mild cognitive impairment
• Oxidative stress markers in brain, including markers for protein oxidation and lipid peroxidation
• Amyloid beta-peptide-mediated oxidative stress and Alzheimer's disease
• Redox proteomics identification of oxidatively modified brain proteins, leading to new insights into protein dysfunction in and neurotoxicity of brain cells in Alzheimer's disease and mild cognitive impairment

Links

Series:

• Free Radicals and the Oxygen Paradox

Categories:

• Biochemistry
• Neuroscience

Therapeutic Areas:

• Neurology

Talk Citation

Butterfield, D.A. (2007, November 1). Oxidative modification of brain proteins in Alzheimer's disease and models thereof: role of amyloid beta-peptide (1- 42) and insights from redox proteomics [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved November 21, 2024, from https://doi.org/10.69645/DCGB4464.
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Publication History

• Published on November 1, 2007
• Archived on October 28, 2018

Financial Disclosures

• Prof. D. Allan Butterfield has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.