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The progressive degeneration of neuronal cells that accompanies the decline of memory and other cognitive functions in subjects with Alzheimers disease is associated with an intracellular aggregation of Tau fibrils, an extra-neuronal accumulation of b-amyloid peptides into senile plaques, and an oxidation-reduction (redox) imbalance of complex etiology

However, despite the promising potential of interventions aimed at correcting metabolic dysfunctions, translating these concepts into practical therapies remains challenging

It plays a critical role in neutralizing free radicals, detoxifying harmful substances, and maintaining cellular health

doi: 10.3390/genes8120398