Understand the neuroimmune basis of neurological diseases using an integrated approach of biological engineering and electrophysiology

Interdisciplinary Areas: Engineering-Medicine

Project Description

Distinct neurological diseases, i.e. Alzheimer’s diseases (AD), and autism spectrum disorders (ASD), shared many aspects of common pathophysiology. It is found that epigenetic changes, altered neuronal excitability and activation of microglia could be convergent mechanisms of these otherwise very different diseases. The Yang and Yuan lab have established multiple mouse models, iPSCs derived neuron/organoid models to study the interactions of neurons and immune systems underlying these diseases. Questions to be addressed in this project include but not limited to: what’s the role of microglia in the maladaptation of altered firing of neurons in the onset of AD, or ASD? What are the neuron or microglia specific epigenetic changes that can be identified in the disease models? Can neuroinflammation or neuroimmune be targeted to provide alleviations of symptoms of AD or ASD?

Start Date

07/01/21

Postdoc Qualifications

Students with a PHD degree in biological science, neuroscience, biomedical engineering, chemical engineering or related disciplines are eligible to apply. Experience with iPSC, microglia or electrophysiology is considered a plus but not required.

Co-Advisors

Chongli Yuan, cyuan@purdue.edu, Chemical Engineering, https://engineering.purdue.edu/ChE/people/ptProfile?resource_id=65069

Yang Yang, yangyang@purdue.edu, Medicinal Chemistry and Molecular Pharmacology, https://www.yangyanglab.org/?_ga=2.209180946.1858684046.1598446041-1432128696.1589815573 

References

Mis MA&, Yang Y&, Tanaka BS, Gomis-Perez C, Liu S, Dib-Hajj F, Adi T, Garcia-Milian R, Schulman BR, Dib-Hajj SD, Waxman SG. Resilience to Pain: A Peripheral Component Identified Using Induced Pluripotent Stem Cells and Dynamic Clamp. Journal of Neuroscience 2019, 39(3):382-392 (&, equal contribution)

Yang Y, Mis MA, Estacion M, Dib-Hajj SD, Waxman SG. Nav1.7 as a pharmacogenomics target for pain: Moving towards precision medicine. Trends in Pharmacological Sciences 2018, 39(3):258-275

Yang Y, Dib-Hajj SD, Zhang J, Zhang Y, Tyrrell L, Estacion M, Waxman SG. Structural modeling and mutant cycle analysis predict pharmacoresponsiveness of a Nav1.7 mutant channel. Nature Communications 2012, 3:1186

Sanchez O, et.al. Profiling Epigenetic Changes in Human Cell Line Induced by Atrazine Exposure. Environ Pollut. 10.1016/j.envpol.2019.113712

Lin L, Xie J, Sanchez OF, Bryan C, Freeman J, Yuan C. Low Dose Lead Exposure Induces Alterations on Heterochromatin Hallmarks Persisting Through SH-SY5Y Cell Differentiation. bioRxiv. 2020:2020.07.27.224246.