Elucidate gene environmental interactions in determining neurodegeneration risk via engineered tools
Interdisciplinary Areas: | Engineering-Medicine, Integrated Neuroscience and Engineering |
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Project Description:
Our collaborative project aims to unravel the epigenetic mechanism contributing to altered synaptic plasticity arising from developmental lead (Pb) and other emerging chemical exposure and when compounded with a genetic risk factors, such as SORL1. We will reveal molecular and cellular features that drive the acceleration of AD onset and progression induced by Pb neurotoxicity via a combination of state-of-the-art sequencing and imaging tools.
Start Date:
02/01/2023
Postdoc Qualifications:
A competitive candidate should have PhD in chemical engineering, biological engineering, health science or a related life science discipline. Prior experience working with hiPSC-derived neuronal culture or zebrafish animal model will be a plus.
Co-Advisors:
Chongli Yuan, cyuan@purdue.edu, Davidson School of Chemical Engineering
Jennifer L Freeman, jfreema@purdue.edu, School of Health Science
Bibliography:
1. Wang S, Bryan C, Xie J, Zhao H, Lin L, Tai JAC, Horzmann KA, Sanchez O, Zhang M, Freeman JL, Yuan C. Atrazine exposure in zebrafish induces aberrant genome-wide methylation. Neurotoxicology and teratology. 2022:107091.
2. Lin, L. F.; Xie, J.; Sánchez, O. F.; Bryan, C.; Freeman, J. L.; Yuan, C., Low dose lead exposure induces alterations on heterochromatin hallmarks persisting through SH-SY5Y cell differentiation. Chemosphere 2021, 264, 128486.
3. Zhao H., Ma D., Xie J., Sanchez O., Huang F., Yuan, C., Live-cell probe for in situ single-cell monitoring of mitochondrial DNA methylation, ACS Sensor, 2021: 10: 3575
4. Xie J, Lin L, Sánchez OF, Bryan C, Freeman JL, Yuan C. Pre-differentiation exposure to low-dose of atrazine results in persistent phenotypic changes in human neuronal cell lines. Environmental Pollution. 2021;271:116379