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CaMKK2 dysfunction may play an underlying role in this phenomenon as genetic deletion of Camkk2 in hippocampal neurons, myeloid cells and immortalized cell lines (HEK293 and HepG2) results in mitochondrial dysfunction that causes a similar switch in cellular energy generation from oxidative phosphorylation to glycolysis [43, 201, 202]

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The disconnect between preclinical efficacy and human clinical outcomes remains unexplained and represents a significant limitation for potential therapeutic applications