Geromics DRAFT PAGE

Kalia Bennett (PI: Dr. Silvia Stringhini)

My research focuses on understanding pathways through which social and environmental conditions shape health and aging outcomes in early-life. Utilizing multiomic data from the Canadian Healthy Infant Longitudinal Development (CHILD) Study, I aim to analyze how early childhood socioeconomic disadvantage becomes biologically embedded to influence biological mechanisms, including epigenetic aging. This work seeks to connect the external social environment with biological mechanisms underlying health and aging trajectories across the lifecourse. Identifying early-life pathways through which social determinants of health biologically embed can help to inform prevention strategies and reduce health inequities across childhood and the lifespan.

Cecilia Hodson (PI: Dr. Katie Marshall)

My research asks the question of how cold adaptation evolves at the genomic level. To explore this, I compare closely related fly species with varying cold tolerance to identify genetic patterns linked to survival. I then examine the snow fly, which stays active below freezing, to test if these patterns hold. This study will provide us with a better understanding of what molecular mechanisms proceed cold adaptation and how we can identify tolerance in non-model species.

Jenni Nguyen (PI: Dr. Mahmoud Pouladi)

Huntington disease (HD) is caused by a mutation in the HTT gene, but this mutation does not fully explain why symptoms begin earlier or progress more rapidly in some people than others. My project focuses on MED15, a gene that helps regulate gene activity and may also influence how cells manage HD pathology. MED15’s contribution to disease progression in HD remains poorly understood, and this project will determine how MED15 influences neurodegenerative disease mechanisms, with the goal of identifying new biological pathways and potential targets for future therapies.

Fan Mingyang (PI: Dr. James McKendry)

My GerOmics project will explore how physical activity and nutrition influence healthy aging through the gut microbiome and metabolome. Using data from older adults with varying activity levels, including sedentary individuals, recreationally active adults, and masters athletes, I will examine how dietary intake and physical activity are associated with gut microbial composition and metabolomic profiles. By integrating microbiome and metabolomics data with measures of physical function, body composition, and overall health, this project aims to uncover lifestyle-related biological pathways and potential markers that may help explain why some people age more healthfully than others.

Grace Earle (PI: Dr. Nicole Templeman)

Modern diets are composed of calorie-dense, high-sugar foods that have direct negative implications for metabolic health and the age-related decline of the female reproductive system. My project will use a mouse model to examine the intergenerational effects of an energy-rich maternal diet and elevated insulin levels on reproductive aging traits of the female offspring. By assessing whether maternal metabolic health leads to changes in ovarian aging for the next generation, my project will generate insights into the far-reaching impacts of metabolic balance and may provide a foundation for exploring genomic mechanisms that perpetuate these effects.

Sara Cristiano (PI: Dr. Stefan Taubert)

As we age, damaged cells can accumulate in the body and, instead of being removed, enter a state called senescence. These cells release signals that promote inflammation and interfere with normal immune function, creating an environment that contributes to the development of age-related diseases such as cancer. My research focuses on a protein called MED15, which helps control what genes are active within a cell. Since gene activity influences the signals produced by cells, MED15 may help shape the inflammatory and immune environment created by these dysfunctional cells. Understanding how MED15 regulates these processes could provide new insights into how aging contributes to diseases like cancer and help uncover new treatment strategies. 

Kenneth Ofori (PI: Dr. Emilia Lim)

Accelerated aging is when a person’s biological age exceeds their chronological age. Climate change has led to wildfires becoming a growing contributor to air pollution, posing health risks to aging and vulnerable populations. Since air pollution and aging are both associated with age-related diseases, we hypothesize that biological age and wood smoke may together worsen outcomes. We will grow donated lung cells and expose them to wood smoke or filtered air, profiling donors’ genomes and gene activity to measure how wood smoke disrupts lung cells and whether aging worsens these effects. Our findings aim to inform health guidelines for aging and at-risk populations.