I am a PhD candidate in the Department of Biochemistry, Molecular Biology and Biophysics/Medical School/Biological Sciences at the University of Minnesota. I work in the lab of Paul D. Robbins.  I have B.S. in Biochemistry from the University of Wisconsin-Madison.

Age is a critical risk factor for the development of multimorbidity of chronic diseases. Numerous studies investigating biochemical changes associated with progressing age have identified multiple drivers of aging including genomic instability, epigenetic remodeling, cellular senescence, and others. These hallmarks are highly interconnected and are thought to be primarily driven by persistent activation of DNA damage and other stress signaling mechanisms that lead to alterations in epigenetic marks and, concomitantly, aberrations in gene transcription that lead to the emergence of harmful aging phenotypes. Further, epigenetic mechanisms contribute to the complexity of targeting aging phenotypes by driving heterogeneity within aging cell populations leading to varying dependencies on regulatory program networks hindering the efficacy of current geroprotective agents. However, ectopic expression of the Yamanaka factors has demonstrated that partial reprogramming for the purpose of cellular rejuvenation downregulated aging phenotypes, restored tissue homeostasis and extended lifespan by means of transcriptional and epigenomic rejuvenation to a younger profile. I aim to better characterize the heterogeneity found in young, aged, and partially reprogrammed cell populations to identify critical epigenetic modulators involved in the development of these cellular phenotypes for the identification of new therapeutic targets and compounds aimed to extend healthspan and simultaneously delay the onset of many chronic diseases. 

The world's health organization anticipates that most of the world's population will live beyond 60 years of age with the population of people aged 80 years or older expected to triple by 2050. This becomes especially important upon the understanding that advancing age is recognized as one of the greatest risk factors associated with the development of chronic disease and multimorbidity. The correlation between age and prevalence of chronic disease leads us to believe that developing therapeutic strategies that target many cellular and molecular mechanisms of aging, like epigenomic modulation, may simultaneously delay the onset of many chronic diseases through healthspan elongation. Geroprotective agents would then serve to prevent the expected increase in socioeconomic burden associated with an ever-aging population and improve the quality of people's lives later in life.

I anticipate using this award largely to for additional hands-on technical and bioinformatic training that would help me advance the analysis of multi-OM IC approaches used in my studies for characterization of various aged and rejuvenated tissues and cell types.

During my graduate career, my goal is to master the execution and analysis of up-and-coming OMIC strategies and develop expertise in aging, cellular senescence, epigenetic modulation, and therapeutic discovery. While my post-graduation plans are under debate, my ultimate career goal is to discover or improve a life-changing drug and be a key driver in helping it reach the hands of those who need it.

I am a first generation American with parents from both the UK and the Philippines. Growing up, I developed a keen interest in plants and phototropism which led me to pursue research in plant pathology at the University of Wisconsin-Madison. After, I ventured into industry where I worked as an analytical chemist optimizing chromatography-based methods for analyte quantification. I have since re-joined academia in pursuit of my PhD specializing in aging and healthspan elongating gerotherapeutics. In my free time, I collect a variety of exotic house plants, I also enjoy going to concerts, Cycle Bar classes, and shopping.