Certain compounds called methoxyphenols inhibit both the amyloid plaque and non-amyloid plaque routes to peroxynitrite formation.

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Furthermore, the peroxynitrite-mediated nitration of tau proteins prevent them from being reconstituted to their normal form.

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One mechanism of oxidative damage is the nitration of tyrosine residues in proteins, mediated by peroxynitrite breakdown.

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Peroxynitrite, a reaction product of nitric oxide and superoxide radicals, has been implicated in N-methyl-D-aspartate receptor-mediated excitotoxic damage.

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Although carbonyl formation is a major oxidative modification induced by peroxynitrite, nitration of tyrosine residues is an indicator of peroxynitrite involvement.

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And the peroxynitrite-mediated nitration of NMDA receptors leads to the release of glutamate and the influx of calcium which kills brain cells.

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Peroxynitrite is a source of hydroxyl radical-like reactivity, and it directly oxidizes proteins and other macromolecules with resultant carbonyl formation from side-chain and peptide-bond cleavage.

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The use of peroxynitrite scavengers partially reverses all of these problems.

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One can easily overcomplicated this disease or oversimplify it (in the case of the amyloid hypothesis), but there is often one causal factor (bacteria, virus, peroxynitrite, etc.) that explains the great majority of diseases and once you identify that factor and how to neutralize it, then you can successfully treat the disease.

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