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AST has been shown to influence core pathological mechanisms in neurodegenerative disease (e.g., AD), including the reduction of tau hyperphosphorylation and suppression of BACE1 activity, both of which are key contributors to neurofibrillary tangle formation and A production, respectively (Table 2

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SS-31 interacts with cardiolipin to maintain cristae structure, supporting studies of mitochondrial integrity in ischemiareperfusion models

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