Project Description

The goal of our work is to identify and validate environmental chemical-interacting genetic risk factors contributing to the etiology of ADRD in “age”-matched human neuronal models. Our study will use hiPSC derived neurons as a model system to identify driving gene-environmental interactions in the establishment of an ADRD-like phenotype.

Start Date

06/01/2025

Post Doc Qualifications

Prior experience with human stem cell culture and a PHD in biological engineering or related fields.  

Co-Advisors

Chongli Yuan, Davidson School of Chemical Engineering, https://engineering.purdue.edu/ChE/people/ptProfile?resource_id=65069
Jennifer Freeman, School of Health Sciences, https://hhs.purdue.edu/directory/jennifer-freeman/

Bibliography

1. Xie J, Wu S, Szadowski H, Min S, Yang Y, Bowman AB, Rochet J-C, Freeman JL, Yuan C, Developmental Pb exposure increases AD risk via altered intracellular Ca2+ homeostasis in hiPSC-derived cortical neurons, Journal of Biological Chemistry, 2023; 299(8):105023
2. Zhao H, Xie J, Wu S, Sánchez OF, Zhang X, Freeman JL, Yuan C. Pre-differentiation exposure of PFOA induced persistent changes in DNA methylation and mitochondrial morphology in human dopaminergic-like neurons. Environ Pollut. 2022;308:119684
3. Zhao, H. et al. Elevated parkinsonism pathological markers in dopaminergic neurons with developmental exposure to atrazine. Sci Total Environ 908, 168307, doi:10.1016/j.scitotenv.2023.168307 (2024)