Donna M. Wilcock (United States of America)
University of Kentucky
Sanders-Brown Center on Aging
Donna M. Wilcock, PhD, is the Robert P. and Mildred A. Moores Endowed Chair in Alzheimer’s Disease at the Sanders-Brown Center on Aging and Professor in the Department of Physiology at the University of Kentucky. She also serves as Assistant Dean of Biomedicine in the College of Medicine. Dr. Wilcock was received her Bachelor’s degree in Pharmacology from Cardiff University. She obtained her Ph.D. at the University of South Florida, and completed postdoctoral training at Albert Einstein College of Medicine and Duke University. Her research is focused on vascular cognitive impairment and dementia (VCID), a common cause of dementia and frequent co-morbidity with Alzheimer’s disease pathology. She is performing translational research on VCID, ranging from studying molecular mechanisms through identification of novel biomarkers in patients. She is primarily focused on inflammatory and angiogenic processes, as well as studying the influence VCID has on the progression and severity of Alzheimer's disease. In addition, Donna serves as the Biomarker Core Director for the University of Kentucky Alzheimer’s Disease Research Center. Her work is funded by the National Institute on Aging and the National Institute on Neurological Disorders and Stroke.

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 Conference Calendar

PRE-RECORDED: PLASMA BIOMARKER IDENTIFICATION FOR DEMENTIA-CAUSING PATHOLOGIES IN A LONGITUDINAL AGING COHORT WITH AUTOPSY

Session Name
0190 - FLUID BIOMARKERS 1 (ID 4)
Session Type
SYMPOSIUM
Date
Wed, 16.03.2022
Session Time
08:30 AM - 10:30 AM
Room
ONSITE PLENARY: 115-117
Lecture Time
10:15 AM - 10:30 AM
Presenter

Abstract

Abstract Body

The study of plasma biomarkers for Alzheimer’s disease (AD) has accelerated greatly in recent years thanks in part to ultra-sensitive, reliable analytic platforms and imaging biomarkers like amyloid and tau-PET. We report here our plasma biomarker findings from a well characterized autopsy cohort.

We identified 90 autopsy cases that had banked plasma within two years of death. We then assayed the last plasma sample prior to death for a battery of biomarkers using Quanterix Simoa assays. Specifically, we measured Aβ40, Aβ42, tau, pTau181, NfL, TNFα, IL6, IL10, GFAP, TGFβ, IL8, MMP9, VEGF-A, PlGF. After log-transforming the data, proportional odds and binary regression models were used to evaluate the relationship between plasma biomarkers and different vascular and AD neuropathological hallmarks. All models were adjusted for age at autopsy and covariates including ApoE genotype, sex, diabetes, and hypertension were included.

Of the AD pathological hallmarks of amyloid plaques and neurofibrillary tangles, we found that the tau/Aβ42 ratio had the greatest association with increased Aβ deposition (Thal score) and neuritic plaques (CERAD neuritic plaque score). In addition, Aβ42/Aβ40 ratio was inversely associated with Aβ deposition and neuritic plaques. Surprisingly, plasma GFAP was associated with Thal and CERAD neuritic plaque scores. Angiogenic factors PlGF, and to a lesser extent VEGF, were associated with worsening CAA, but showed a modest inverse association with arteriolosclerosis and chronic cerebrovascular pathologies.

Overall, we were able to confirm associations of candidate plasma biomarkers with AD pathologies in a well-characterized autopsy cohort and identify unique biomarker changes associated with cerebrovascular pathologies.

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