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Engineering | School of Biological and Health Systems Engineering

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Date/Time
Date(s) - 09/10/2021
3:05 pm - 4:05 pm

Category(ies)


Vital Cell Types & Signals in Human Cortex Development & Disease

Speaker:
Madeline Andrews, Ph.D.
Assistant Professor in the School of Biological & Health Systems Engineering, Arizona State University

Date: Friday, September 10, 2021
Time: 3:05 p.m.
Location: SCOB 228

Flyer

Abstract

The cerebral cortex is expanded in humans and this increase in size, cellular diversity, and complex organization are vital for cognitive function. The origin of cortical cellular diversity is established during gestation and disruption to early cortical organization can result in devastating neurodevelopmental diseases. My scientific goal is to understand the relevant signaling mechanisms, cellular interactions and metabolic programs required for fate specification in the human cortex and how disruption impacts onset of neurological disease. My current research seeks to evaluate the fidelity of in vitro model systems and gain insight into features of human development from current model limitations. Additionally, I am exploring how particular signaling activity becomes dysregulated in neurodevelopmental disorders and the impact on development of human neural cell types. In these studies, I utilize cortical organoid models and transcriptomic approaches to evaluate features of human brain development and implications for disease.

Bio Sketch

Madeline Andrews is an incoming assistant professor in the School of Biological & Health Systems Engineering where she will be starting her lab in January 2022. She received her PhD in Neuroscience in 2017 from University of California, Los Angeles and her BS in Psychology from ASU in 2010. She completed her postdoctoral training at the University of California, San Francisco where she studied human cortical development in Dr. Arnold Kriegstein’s lab. Her lab will utilize neural organoids, transplantation models, and omics approaches to study human brain development and disease.