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The mechanism the clinic describes is that MOTS-C works by activating AMPK, a key metabolic pathway involved in glucose utilisation, fat oxidation and insulin sensitivity

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In recent years, two major intervention strategies have demonstrated significant neuroprotective potential in preclinical models: synthetic small-molecule inhibitors (such as ferrostatin-1, liproxstatin-1, and iron chelators) and naturally derived small molecules (such as curcumin, resveratrol, baicalein, and ginsenosides)