Oxidative damage is a major feature of Alzheimers disease pathophysiology. Instead of succumbing to these oxidative abnormalities, neurons upregulate antioxidant defenses, which suggest a novel balance in oxidant homeostasis in Alzheimers disease. Evidence indicates that in the initial phase of Alzheimers disease development, amyloid-β deposition and hyperphosphorylated τ are consequences of oxidative stress and function as a primary line of antioxidant defense. However, during the progression of the disease, the antioxidant activity of both agents evolves into pro-oxidant, representing a typical gain-of-function transformation. This transformation is due to an increase in reactive species and a decrease in clearance mechanisms. However, the notion that amyloid-β and hyperphosphorylated t function as protective components in the early stages of Alzheimers disease brings into serious question the rationale of current therapeutic strategies aimed to remove both amyloid-β and hyperphosphorylated τ.
Keywords: alzheimer disease, amyloid, oxidative stress, reactive oxygen species, tau
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