In our investigations of the modulator mechanisms driving the respiratory abnormalities, we observed that the AD-A LCLs, as compared to AD-N LCLs, failed to upregulate key regulators of mitochondrial biogenesis and homeostasis—specially PINK1, MFN2, SIRT1, SIRT3 DNM1L, HIF1z and PGC1a [12]. The gene discussed is PPARGC1A; the disease is Alzheimer disease.