All these impairments and abnormalities lead to increases in the circulating C reactive protein, IL-6 [34,35], TNF-α and its receptors [36], intercellular adhesion molecule 1 (ICAM-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), the astrocytic intermediate filament glial fibrillary acidic protein (GFAP), and markers of mitochondrial dysfunction, such as growth/differentiation factor 15 (GDF15) and fibroblast growth factor 21 (FGF21) [37], translated clinically into physical frailty and sarcopenia [37]. This evidence concerns the gene GFAP and sarcopenia.