Tuesday, 17 October 2006
Salon D-E (Doubletree Hotel at Reid Park)
415

Complexation of Beta-Amyloid and Iron(III)

Renee T. Williams1, Dianlu Jiang1, Feimeng Zhou1, Lijie Men2, and Yinsheng Wang2. (1) California State University, Los Angeles, Los Angeles, CA, (2) University of California, Riverside, Riverside, CA

Alzheimer's disease (AD) is a progressive, neurodegenerative disorder characterized by the deposition of amyloid plaque.  The plaque is primarily composed of insoluble beta-amyloid (Aβ) protein fibrils and metals at elevated concentrations.  In a human brain, the neurotoxicity of Aβ plaque has been suggested to originate from a Fenton-like reaction wherein the peptide-metal complex(es) is(are) involved in the generation of  reactive oxygen species.  To date, the majority of studies have focused on Aβ-copper and Aβ-zinc interactions, whereas Aβ-iron complexes have not been extensively investigated.  As such, the objective of this research is to 1) use mass spectrometry and spectroscopic techniques to study the Aβ-iron complex formation and 2) to show that the Aβ-iron complex is redox-active.  We will correlate our results obtained in vitro to in vivo observations and attempt to provide insight to the understanding of the Aβ aggregation process and its possible link with oxidative stress.

 


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Back to The 19th Rocky Mountain Regional Meeting (October 14-18 2006)