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This is attributed to the loss of MT stabilization and even destabilization of MTs, and also destabilizing interactions with actin filaments, as the phosphorylation of Tau at specific sites reduces the capacity of Tau to bind MTs that contributes to neuronal structural instability and neurodegeneration (Johnson and Stoothoff, 2004

A possible explanation for this phenomenon is that these subjects are at maximum physiologic compensation with a high baseline oxidative burden