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Register: Webinar on Neuroimmune Models for Alzheimer’s Risk

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Wild type human iPSC-derived microglia (green) responding to amyloid plaques (red)

Learn about recent research characterizing potential roles of Alzheimer’s risk gene TREM2 in activating immune responses in the brain.

Join us for a webinar with Amanda McQuade of Dr. Mathew Blurton-Jones’s lab! McQuade and the lab have developed protocols for differentiating microglia from induced pluripotent stem cells (iPSCs) and use these microglia in various ways to understand mechanisms of neurodegeneration.


TITLE

“Modeling Alzheimer's risk using human TREM2-knockout microglia”

DATE & TIME

There are multiple sessions for this global event - Please choose the one that best fits your local time of day.

Tuesday, January 26, 2021
Session 1: 9:00 a.m. PST | 12:00 p.m. EST | 6:00 p.m. CET

Tuesday, January 26, 2021
Session 2: 6:00 p.m. PST (Please note that this is Wednesday, January 27, 10:00 a.m. China Standard Time | 11:00 a.m. JST | 12:00 p.m. AEST)

ABSTRACT
Unbiased studies of Alzheimer's disease risk loci have revealed a strong enrichment for loci proposed to affect immune function. At the forefront of these new risk loci is Triggering Receptor Expressed on Myeloid Cells 2 (TREM2). Loss of function of TREM2 increases Alzheimer’s disease risk, though the mechanism for this increased risk is not completely understood. We have modeled TREM2 loss of function through isogenic CRISPR-knockout of TREM2 in iPS-derived human microglia. Through a combination of in vitro mechanistic studies and xenotransplantation into a chimeric model of Alzheimer's disease, we show that human TREM2-knockout microglia fail to properly activate towards disease pathology, suggesting a mechanism for increased risk of Alzheimer's disease.

Interested in learning more but unable to attend the event online? Register now and you will be notified when the recording is available.

Amanda McQuade
PhD Candidate, Mathew Blurton-Jones lab, Institute for Immunology
University of California, Irvine