Abstract

Proper distribution of mitochondria in axons and dendrites is crucial for many neuronal functions. Work in cell culture and intact organisms suggests that early decline of mitochondrial axonal transport is a hallmark of ageing and neurodegeneration. Although reduced transport contributes to the broader decline of neuronal homeostasis that occurs during ageing, it is still unclear how decline in motility mechanistically affects ageing and neurodegenerative phenotypes. Mounting evidence supports the idea that mitochondrial transport and function are mechanistically linked. Thus, halting motility would likely be followed by a rapid functional response. However, this hypothesis has not been extensively tested, partly due to the lack of suitable systems to inhibit the transport of mitochondria with high spatiotemporal precision. Despite the growing array of optogenetic tools, ways to interfere with the mitochondrial transport machinery at the endogenous level in vivo are currently scarce. During my talk I will discuss our current approaches to this complex problem, including introducing new tools that we are developing in order to interfere with mitochondrial motility and function with high spatiotemporal precision.