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Functional rescue experiments demonstrated that LONP1 gene silencing recapitulates AD-associated mitochondrial protein homeostasis defects and dysfunction, while exogenous overexpression of LONP1 not only reverses A42-induced mitochondrial dysfunction but also significantly improves cognitive deficits in AD mice [31]

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Gene expression analyses further show upregulation of antioxidant-response elements, reinforcing mechanistic consistency at both biochemical and transcriptional levels

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