Consistently, a number of genetic aberrations causing ALS, FTD, and CMT sensorimotor axonal neuropathy were shown to compromise mitochondrial function, e.g., the GGGGCC repeat expansion in C9orf72 [31], VCP (valosin containing protein) mutations [32], CHCHD10 (coiled-coil-helix-coiled-coil-helix domain containing 10) mutations [33,34], and DYNC1H1 (dynein cytoplasmic 1 heavy chain 1) mutations [35,36]. This evidence concerns the gene DYNC1H1 and frontotemporal dementia.