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Zinc may play a role as a co-factor in the pathogenesis of Alzheimer’s disease(AD)through influencing the conformation and neurotoxicity of amyloidβ-protein(Aβ).Using the fluorescamine assay,we show for the first time that Zn~(2+)induced Aβ(10-21) aggregate in a concentration-dependent manner.These results indicate that Aβ(10-21)can be used as an in vitro model in Zn~(2+)- induced Aβaggregation and that the region 10-21 to be the minimal fragment of zinc-binding domain of full length Aβ(1-42).
Zinc may play a role as a co-factor in the pathogenesis of Alzheimer’s disease (AD) through influencing the conformation and neurotoxicity of amyloid beta-protein (Aβ). Using the fluorescamine assay, we show for the first time that Zn ~ (2+ ) induced Aβ (10-21) aggregate in a concentration-dependent manner. These results indicate that Aβ (10-21) can be used as an in vitro model in Zn ~ (2 +) - induced Aβaggregation and that the region 10- 21 to be the minimal fragment of zinc-binding domain of full length Aβ (1-42).