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lüll Targeting Glycogen Synthase Kinase-3beta for Therapeutic Benefit against Oxidative Stress in Alzheimer s Disease: Involvement of the Nrf2-ARE Pathway Kanninen K; White AR; Koistinaho J; Malm TInt J Alzheimers Dis 2011[]; 2011 (ä): 985085Specific regions of the Alzheimer's disease (AD) brain are burdened with extracellular protein deposits, the accumulation of which is concomitant with a complex cascade of overlapping events. Many of these pathological processes produce oxidative stress. Under normal conditions, oxidative stress leads to the activation of defensive gene expression that promotes cell survival. At the forefront of defence is the nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor that regulates a broad spectrum of protective genes. Glycogen synthase kinase-3beta (GSK-3beta) regulates Nrf2, thus making this kinase a potential target for therapeutic intervention aiming to boost the protective activation of Nrf2. This paper aims to review the neuroprotective role of Nrf2 in AD, with special emphasis on the role of GSK-3beta in the regulation of the Nrf2 pathway. We also examine the potential of inducing GSK-3beta by small-molecule activators, dithiocarbamates, which potentially exert their beneficial therapeutic effects via the activation of the Nrf2 pathway.ä |