also serves to repair abnormal mitochondrial phenotypes [45]. The extensive fusion of mitochondria observed at later time points in our studies might indicate a compensatory response to mitochondrial damage. Hyperfused mitochondria may be resistant to apoptosis [46] and escape autophagosomal degradation [47].[48]. Fission, conversely, generates fragmented mitochondria that are necessary for transportation purposes as well as selecting damaged or aged mitochondria for autophagy. Changes in both of these processes have been shown to contribute to neurodegenerative and other disorders [26]. Further, mitochondrial trafficking is important in neurons since active transport of mitochondria supplies local energy needs [49]. Several studies have shown that defects in the microtubule-based machinery can cause or contribute to a number of human neurodegenerative diseases [32, 42, 50-51].
