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There is now a CONTENT FREEZE for Mercury while we switch to a new platform. It began on Friday, March 10 at 6pm and will end on Wednesday, March 15 at noon. No new content can be created during this time, but all material in the system as of the beginning of the freeze will be migrated to the new platform, including users and groups. Functionally the new site is identical to the old one. webteam@gatech.edu
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Name: Ursula Saelzler
Dissertation Proposal Meeting
Date: February 4, 2020
Time: 10:00 am
Location: J.S. Coon Building, Room 150
Advisor:
Scott Moffat, Ph.D. (Georgia Tech)
Thesis Committee Members:
Mark Wheeler, Ph.D. (Georgia Tech)
Thackery Brown, Ph.D. (Georgia Tech)
Paul Verhaeghen, Ph.D. (Georgia Tech)
Matt Panizzon, Ph.D. (UC San Diego)
Title: A longitudinal investigation of cortisol as a driver of amyloid deposition in older adults
Abstract:
Amyloid β (Aß) deposition has been considered a hallmark of Alzheimer’s disease (AD) since its initial description at the start of the 20th century. Nearly 100 years later, the advent of the positron-emission tomography (PET) radiotracer Pittsburgh Compound-B (PIB) enabled the in vivo measurement of amyloid deposition. Research using PIB has demonstrated that Aß accumulation may begin nearly two decades before clinical diagnosis of AD and that greater deposition increases risk for the development of sporadic AD in older adults. The utility of PIB measured during this preclinical phase to predict AD onset coupled with the failure of anti-amyloid treatments targeted at individuals diagnosed with AD or mild cognitive impairment (MCI) has spurred research aimed at determining factors which may influence amyloid deposition, particularly during the preclinical phase. In recent years, the steroid hormone cortisol has been proposed as a stimulant of Aß accumulation on the basis of in vitro and rodent studies. The proposed study would represent the first longitudinal investigation of the relationship between cortisol and Aß accumulation in humans, using the changes to changes extension of the bivariate latent difference score model to test whether changes in cortisol precede changes in Aß deposition in vivo.
