About Sung M Han
Neurons extend axons and form synapses to communicate with distant cells. These unique structures are susceptible to damage from pathological or physiological stresses. Despite their delicate structure, most neurons are not replaced, and so they must be maintained throughout the life of the animal. My long-term research goal is to understand how the nervous system maintains its function and integrity during aging. In particular, my current goal is to identify mechanisms that regulate the location and function of the mitochondria in two key neuronal conditions: injury (the regulation of axon regeneration) and maintenance (preserving normal synaptic function). In response to a range of conditions, neurons transport and position mitochondria at distinct subcellular sites within axons and synapses. Incorrect mitochondrial localization in neurons can result in functional deficits, failure of axon regeneration, and neurodegeneration. However, the mechanisms that regulate mitochondrial localization, and how mitochondrial subcellular localization supports specific neuronal functions are incompletely understood.
My specific goals are:
1) Investigate how aging neurons regulates mitochondrial dynamics in response to local demand and injury; 2) Elucidate how mitochondria control nuclear gene expression in aging neurons; 3) Discover how aging neurons maintain mitochondrial function at synapses.
Over the long term, I believe that these approaches will result in a new understanding of the mechanisms that maintain optimal function of the nervous system during aging by regulating mitochondrial function in aging/stressed neurons. My lab’s findings will provide better insight into novel therapeutic approaches to restore neuronal functional after nerve injury that can cause permanent loss of motility and disability.