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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]

Chen T, Tanaka M, Wang Y, Sha S, Furuya K, Chen L, et al

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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

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