OXIDATIVE STRESS INDUCES DEPHOSPHORYLATION OF TAU IN RAT-BRAIN PRIMARY NEURONAL CULTURES

Oxidative stress and free radical damage have been implicated in the n eurodegenerative changes characteristic of several neurodegenerative d iseases, including Alzheimer's disease. There is experimental evidence that the neurotoxicity of beta-amyloid is mediated via free radicals, and as the deposition of beta-amyloid apparently precedes the formati on of paired helical filaments (PHF) in Alzheimer's disease, we have i nvestigated whether subjecting primary neuronal cultures to oxidative stress induces changes in the phosphorylation state of the principal P HF protein tau that resemble those found in PHF-tau. Contrary to causi ng an increase in tau phosphorylation, treatment of neurones with hydr ogen peroxide caused a dephosphorylation of tau and so we conclude tha t oxidative stress is not the direct cause of tau hyperphosphorylation and hence of PHF formation.