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This work underscores a physiologic role for mitochondrial fragmentation as a basic mechanism whereby cellular fuel preference and FAO capacity are determined.

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Its ability to penetrate the BBB, its metabolic stability, and its significant efficacy in restoring cognitive and motor functions in animal models of AD and PD, likely through modulating the HGF/c-Met system, position it as a highly promising therapeutic candidate for these debilitating neurodegenerative diseases [2]