Abstract
Reacted with methylglyoxal (MGO), murine Aβ(1-40) (mAβ) produced significantly less superoxide anion (O2•–) compared to human Aβ(1-40) (hAβ). The reactions of MGO with mAβ(R13H), hAβ(H13F), Nα-acetyl-l-lysine, and Nα-acetyl-l-arginine implied that the lack of His13 in mAβ prohibits its Lys16 residue from reacting to produce cross-linked reaction products and O2•–. Our results suggest that murine brains are under less oxidative stress than human brains, which may be one of the reasons why rodents do not develop AD-like symptoms, and which provides further insight into a chemical mechanism for the development of AD in humans.
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