Role of Oxygen Radicals in Alzheimer’s Disease: Focus on Tau Protein

Oxygen free radical burst is a prominent early event in the pathogenesis of Alzheimer’s disease (AD). Posttranslational modifications Tau protein, primarily hyper-phosphorylation and truncation, are indicated as critical mediators AD pathology. This finding confirmed by high levels oxidative stress markers increased susceptibility to oxygen radicals found cultured neurons brains from transgenic animal models expressing toxic forms, concomitance with dramatic reduction their viability/survival. Here, we collect latest progress research focused on reciprocal dynamic interplay between pathological Tau, discussing how these harmful species cooperate and/or synergize progression AD. In this context, better understanding role determining pathology, vice versa, could be able define novel biomarkers stages human tauopathies, including AD, then develop therapeutic strategies aimed at attenuating, halting, or reversing progression.