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Printable Handouts
Navigable Slide Index
- Introduction
- Free radical oxidative stress
- Brain is poised for oxidative damage
- Radicals formation can lead to proteins damage
- Protein oxidation: assessed by protein carbonyls
- Lipid peroxidation
- Formation of 3-nitrotyrosine (1)
- Formation of 3-nitrotyrosine (2)
- Alzheimer's disease (AD)
- Characteristics of Alzheimer's disease
- Aging - the biggest risk factor for AD
- Slice of an AD brain
- Senile plaques
- From amyloid-precursor-protein to amyloid-beta
- Amyloid-beta peptide
- Abeta(1-42) is central to the pathogenesis of AD
- AD brain is under oxidative stress
- Model for AD pathogenesis
- ROS production by Abeta(1-42)
- Abeta (1-42) causes neuronal protein oxidation
- Abeta(1-42) causes loss of CK and GS activities
- Abeta(1-42)-induced lipid peroxidation
- Abeta(1-42) causes HNE formation
- Michael addition process
- HNE formation can lead to proteins damage
- Modification of ion-motive ATPases by HNE
- Modification of GLT-1 by HNE
- Glutamate-induced excitotoxicity
- HNE and acrolein
- Detoxification involving MRP-1
- GST and MRP-1 are oxidatively modified by HNE
- Prediction
- Abeta(1-42) addition leads to Ca accumulation
- What is the mechanism of calcium accumulation?
- Methionine is key to Abeta(1-42)-induced effect
- Results of mutation in Met35 of Abeta(1-42)
- Protein oxidation in transgenic C. elegans
- Formation of sulfuramyl free radical
- Met radical-induced protein/lipid oxidation
- Importance of Abeta(1-42) secondary structure
- Results of disrupting the secondary structure (1)
- Results of disrupting the secondary structure (2)
- Sulfuranyl free radical in Abeta peptides
- Loss of oxidative toxicity of Abeta (1-42)
- Hypothesis
- Human Abeta(1-42) expressed in C.elegans
- Assessment of protein oxidation using the model
- Amyloid deposits using X-34
- Abeta toxicity and aggregates of the peptide
- Oxidative stress in mild cognitive impairment brain
- Oxidative stress is an early event in AD
- Lipid peroxidation in MCI brain
- 3-NT levels in MCI brain
- Location of senile pluqes in an AD brain
- Redox proteomics
- Proteomics and disease
- Book about redox proteomics
- First use of proteomics in AD
- Proteomics and oxidative modifications in AD
- 2-dimensional gel electrophoresis
- Identification of oxidatively modified proteins (1)
- Identification of oxidatively modified proteins (2)
- MS analysis and probability plots of three proteins
- Proteins identified in Butterfield laboratory
- Classification of the identified proteins by function
- Oxidatively modified PIN-1 in AD brain
- PIN-1 and AD
- PIN-1 structure
- Redox proteomics of MCI brain
- Oxidatively modified proteins in MCI hippocampus
- Elevated levels of cell cycle proteins in MCI brain
- Proteins important in conversion from MCI to AD
- Recapitulation of the identified proteins
- Identification of oxidized proteins in vivo
- Groups of proteins identified by proteomics
- Protein oxidation and Abeta(1-42) expression
- The C.elegans Abeta(1-42) proteomics study
- Proteomics analysis of brain in canine model
- Why the canine model?
- Diet treatment
- Behavioral enrichment
- Hypothesis of the aging Beagle study
- Decreased protein oxidation in aged Beagles
- Increased antioxidant enzyme activity after EA
- EA increased expression of neuroprotective HO-1
- Cu, Zn-SOD and GAPDH expression
- Identification of oxidized proteins in aged Beagles
- Summary of the Beagle study results
- Implications for reducing risk for AD development
- Cellular processes leading to neurodegeneration
- Redox proteomics analysis - other disorders
- Summary: Abeta(1-42) induction
- Summary: Abeta(1-42) and oxidative stress
- Summary: Abeta(1-42) forms reactive alkenals
- Summary: Abeta(1-42) excitotoxic mechanisms
- Summary: proteomics
- Summary: modified proteins
- Summary: Abeta peptide-oxidative stress model
- Recapitulation of the AD pathogenesis model
- 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
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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 October 12, 2024, from https://doi.org/10.69645/DCGB4464.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. D. Allan Butterfield has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
Oxidative modification of brain proteins in Alzheimer's disease and models thereof: role of amyloid beta-peptide (1- 42) and insights from redox proteomics
A selection of talks on Biochemistry
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