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"Pulse-chase proteomics of App Knock-In mice reveals synaptic dysfunction may originate in presynaptic terminals during Alzheimer’s disease" by Jeffrey N. Savas, PhD Assistant Professor, Department of Neurology, Northwestern University, Feinberg School of Medicine

Event Type
Seminar/Symposium
Sponsor
Neuroscience Program
Virtual
wifi event
Date
Nov 10, 2020   4:00 pm  
Speaker
Jeffres Savas, Northwestern Medicine
Registration
Registration
Contact
Anna Kukekova
E-Mail
avk@illinois.edu
Views
55
Originating Calendar
Neuroscience Program Seminars

Compromised protein homeostasis underlies accumulation of plaques and tangles in Alzheimer’s disease (AD); however, little is known about the early mechanisms that contribute to this process.  To objectively assess protein turnover at early stages of amyloid beta proteotoxicity, we used dynamic 15N metabolic labeling followed by proteomic analysis of amyloid precursor protein knock in mouse brains. Our findings reveal that the presynaptic terminal is particularly vulnerable and represents a critical site for manifestation of initial AD etiology.

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