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Reframing the conceptual paradigm from a reductionist focus on liver flushing toward the targeted support and optimization of glutathione-dependent detoxification pathways establishes a model primarily oriented around the promotion and maintenance of cellular resilience

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hereditary disease linked to mutated genes encoding amyloid precursor protein APP, presenilins1 and 2, and tau protein) and late onset sporadic forms for which age is the main risk factor