Mitochondria are often referred to as the “powerhouse of the cell.” However, for something important enough to gain that kind of reputation, we still have much to learn about the various roles mitochondria play in humans.

One of the most striking features of neurons is the extraordinary structural and functional compartmentalization of their somatodendritic and axonal domains. They use this high degree of polarization to receive electrical and chemical information from many other neurons, integrate it, and then transmit this information to their synaptic partners. Recent work has revealed that the specific localization of mitochondria is required for both axonal and dendritic development and maintenance.

Many studies claim that reduced mitochondrial motility is a main player in multiple neurodegenerative diseases; yet, most of these studies were performed using immature cultured neurons. We now know that mitochondrial motility is actually extremely low in healthy, mature adult axons and dendrites in vivo. This suggests the need for a complete re-evaluation of the role of mitochondria trafficking in neurodegenerative disease progression. It is imperative that we develop tools and methods to study these processes in vivo.

Our work focuses on two main questions:

1. What are the cellular and molecular mechanisms that regulate compartmentalized morphology and function of mitochondria in neurons?
2. How are these mechanisms altered during the early stages of neurodegeneration, and how does this contribute to reduced neuronal function and degeneration?

We use a suite of genetic, cellular and molecular tools, including in vivo 2-photon imaging, in utero electroporation, viral transduction and proteomics to probe these questions.

Our long-term goal is to understand the physiological role of mitochondria in neuronal function and disease, and to identify novel therapeutic targets for the treatment of these diseases.

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