Kate E. Foley, PhD

Bio

Most neurodegenerative diseases are extremely complex and stem from both genetic and environmental factors that influence disease progression.

During her undergraduate career at SUNY Binghamton, she identified candidate genes that altered susceptibility to a Parkinson’s disease-inducing herbicide, paraquat, and that this genetic susceptibility was sex-specific. 

Kate acquired her PhD in Mammalian Genetics through Tufts University with her research taking place at The Jackson Laboratory in Bar Harbor, Maine. Her thesis centered around using both genetic (APOEε4) and environmental (physical inactivity) risk factors in mouse models to better understand how they influence peripheral (blood) and central (brain) risk factors for Alzheimer’s Disease (AD). She has found that there are important differences between the number of APOEε4 alleles (APOEε4 dosage) and this directly affects how chronic running influences both peripheral and central AD risk factors. 

Her postdoc started at University of Kentucky followed by a move to Indiana University. Kate aims to understand the underlying mechanisms of the devastating and common adverse effects associated with anti-Aβ immunotherapies called amyloid related imaging abnormalities (ARIA). She is utilizing genomics, imaging, and histochemistry to elucidate how glial cells contribute to ARIA in hopes to in the future improve these AD-modifying drugs.