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The multi-domain therapeutic potential inferred from our surrogates should be viewed within the limitations of the scopolamine model as not replicating synaptic failure, progressive neurodegeneration, and proteinopathic features typical of AD

Inflammation and the pathogenesis of atrial fibrillation

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In vitro, Mfn2 reconstitution enhanced mitochondrial membrane potential, mitigated oxidative stress, and promoted fusion-mediated mitochondrial function in cardiomyocytes exposed to high-glucose/HFD conditions, highlighting the regulation of Mfn2 as a promising therapeutic target in DbCM [69]