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In their study, first author Dr. Markus P. Kummer and colleagues discovered that amyloid beta(AΒ) is a novel nitric oxide(NO) target. They observed nitrated AΒ in Alzheimer's disease(AD) and AD mouse models and found that this modification accelerated the deposition of human AΒ. Importantly, reduction of nitric oxide synthase(NOS2) reduced AΒ deposition and memory deficits in a mouse model of AD. Further, nitrated AΒ induced the formation of amyloid plaques when injected into the brains of mice with genetic mutations associated with AD.
"Taken together, our results identify a novel modification of AΒ, tyrosine nitration, and propose a causative link between the AΒ cascade, activation of NOS2, and the subsequent increase in its reaction product nitric oxide during AD," concludes Dr. Heneka. "We think that nitrated AΒ may serve as marker of early AΒ plaque formation. More importantly, it may be a promising target for an AD therapy, and that application of specific inhibitors of NOS2 may therefore open a new therapeutic avenue in AD."