Mitochondrial dysfunction is a common characteristic of all neurodegenerative diseases. However, the cause of this dysfunction has remained mystery. One of the emerging theories behind the causes of observed mitochondrial dysfunction has been related with mitochondrial dynamics. All major neurodegenerative diseases are associated with impaired motility and mitochondrial fragmentation, latter related with imbalance of fusion/ fission dynamics. However, current knowledge seems to be limited to say in what extent these two phenomena are related. Could impaired motility be behind observed mitochondrial shortening/fragmentation? Could mitochondrial fragmentation impair somehow mitochondrial motility? Which of these factors is responsible for observed local/global energetic deficit? With the present project I present a hypothesis that changes in mitochondrial motility are leading to decreased mitochondrial fusion rate that in turn results in mitochondrial shortening or fragmentation. I also suggest that mitochondrial fragmentation together with impaired motility rather than altered fusion. rate are direct reasons for bioenergetic deficit resulting to axonal degeneration and neurodegeneration more general.