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Alzheimer's disease (AD) is characterized by cognitive decline due to excess amyloid beta peptide (Aβ), neurofibrillary tangles, and neuronal loss. Aβ promotes neuronal apoptosis in AD by activating glycogen synthase kinase-3β (GSK-3β), leading to degradation of β-catenin and inactivation of Wnt signaling. β-Catenin interacts with the T-cell factor (TCF)/Lymphoid enhancer factor (LEF)-nuclear complex...