In hippocampal progenitor cells from a Down syndrome mouse model and cells derived from patients with Down’s syndrome, EGCG could also sustain and enhance mitochondrial functions by up-regulating PGC-1α/SIRT1/AMPK axis as well as increasing SIRT1-dependent PGC-1α deacetylation [64, 66]. The gene discussed is SIRT1; the disease is Down syndrome.