This is a relatively new area of interest to clinical neurologists. Mitochondrial movement, fusion, intracellular division, and finally a tubular network may be beneficial for transporting mitochondrial to areas of high energy demand. Motor neurons with no anterior horn cells anywhere need mitochondrial movement from the cell body to the neuromuscular junction. In the process, mitochondrial dynamic processes are regulated by GTPase upstream of microtubules, kinesins, and downstream dynein. The first mitochondrial motor defect was found in a family of autosomal dominant SPG10 and kinesin-encoded gene mutations (KIF5A). Gene mutations affect regions involved in microtubule-binding proteins.