Neurons are postmitotic and highly energy-dependent and therefore particularly vulnerable to alterations in cellular bioenergetics and increased stress that may occur as a direct or indirect result of mitochondrial dysfunction. These cellular processes are also implicated in age-related neurodegenerative disorders, such as AD, PD and ALS, indicating a common pathological thread [25-26]. Integral changes in mitochondria have long been thought to contribute to the pathological events during aging, notably in relation to complex I deficiency of the electron chain and the accumulation of mitochondrial DNA (reviewed in [25, 41]). But so far, mitochondrial morphology as well as trafficking within individual neurons has been challenging to study because neuronal processes must be adherent, stable and accessible for high-resolution imaging.
