Research: In my thesis work, I aim to understand the underlying causes of systemic age-
associated phenotypes in mice, including cell senescence, cell exhaustion, and inflammaging, characterized by a basal increase in inflammatory cytokines like TNFa and IFNg. My current interests lie in the aged bone marrow, where hematopoietic stem cells skew toward the myeloid lineage and away from the
lymphoid lineage, promoting the production of inflammatory cells capable of
seeding tissues throughout the body. Using bone marrow chimeras, it is possible
to understand the downstream effects of hematopoietic aging and subsequent
myeloid skewing, including the distinction between cell-intrinsic and environmental aging defects. In doing this work, I aim to identify a novel age-associated pathway of dysfunction that could be targeted to protectively mediate adverse aging pathologies.
