Another extraordinary parallelism between LPS and aging is the drop in PGC-1α, along with sometimes rescue by a rise in PGC-1α, which has been observed and incriminated in aging [20] and the development of many aging-related disorders including obesity and type 2 diabetes [21, 22], coronary diseases [23], neurodegenerative disorders (Alzheimer [24, 25], Parkinson [26–28], and Huntington [29–31] diseases), myocardial infarction [32–37], mitochondrial dysfunction in senescent brain [20, 38, 39], and stroke [40–43]. This evidence concerns the gene PPARGC1A and glycogen storage disease VI.