Aging is a fundamental biological reality that is familiar to all of us. But how do organisms age at the molecular level? Several genes and processes have been identified that affect the rate of aging, many of which play important roles in highly conserved signaling pathways with relevance to age-related diseases like cancer and neurodegeneration. However, how these processes and conserved genes affect aging at the cellular and molecular level to influence organismal aging is not fully understood. The Hansen lab's research is directed towards understanding the molecular mechanisms that affect the process of aging.
Using a combination of genetic, cytological and biochemical approaches in the genetically tractable model organism C. elegans as well as in mammalian cell culture, we focus on unraveling how several evolutionarily conserved signaling pathways and processes modulate organismal aging.
A particular focus of the lab is to understand the role of autophagy, a basic cellular process by which cytosolic components are being degraded and recycled (Figure 1), in organismal aging. Autophagy has been linked to many age-related diseases as well as aging, and new molecular insights on how autophagy functions in aging may facilitate future treatments of age-linked disorders, including cancer and neurodegenerative diseases.