CHANGE IN ALZHEIMER’S DISEASE BLOOD-BASED BIOMARKERS AND ASSOCIATIONS WITH CORTICAL THICKNESS

Q: What was the main goal of the study?

To determine how changes in blood-based biomarkers of Alzheimer’s disease relate to late-life cortical thickness in community-dwelling populations.

Q: How were cortical thickness and biomarkers measured?

Cortical thickness was quantified from 3T MRI using FreeSurfer, and midlife and late-life plasma samples were assayed in 2022 with Quanterix SiMoA for Aβ42/40, p-Tau181, NfL, and GFAP.

Q: Which biomarker changes were linked to cortical thinning in late life?

Higher midlife p-Tau181 and increases from midlife to late-life in NfL and GFAP were associated with lower cortical thickness in late life.

Sep 28, 2026

Upload by Maya Linwood

Blood-based biomarkers offer a noninvasive way to monitor Alzheimer’s disease pathology and neurodegeneration across the lifecourse. The study evaluates whether longitudinal changes in these biomarkers relate to late-life brain morphology in community-dwelling adults. From 2011 to 2013, 1,977 participants underwent 3T MRI and whole-brain cortical thickness quantification with FreeSurfer. Plasma collected in midlife (1993–95) and late-life (2011–13) was assayed in 2022 for Aβ42/40, p-Tau181, NfL, and GFAP using Quanterix SiMoA.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages1

Reading Time3 min

AccessFree to download

Abstract

Biomarkers and imaging approach

Study design and analytical models

Key associations and age-stratified findings

Need for further longitudinal research

64 Innovation in Aging, 2025, Vol. 9, No. S2 Abstract citation ID: igaf122.210 CHANGE IN ALZHEIMER’S DISEASE BLOOD-BASED BIOMARKERS AND ASSOCIATIONS WITH CORTICAL THICKNESS James Pike1, Yifei Lu2, Keenan Walker3, Thomas Mosley4, Rebecca Gottesman5, Clifford Jack6, Josef Coresh1, and Priya Palta7, 1. New York University, New York, New York, United States, 2. Merck, Landsdale, Pennsylvania, United States, 3. National Institute on Aging, Baltimore, Maryland, United States, 4. University of Mississippi Medical Center-The MIND Center, Jackson, Mississippi, United States, 5. National Institutes of Health, Bethesda, Maryland, United States, 6. Mayo Clinic, Rochester, Minnesota, United States, 7. University of North Carolina School of Medicine, Chapel Hill, North Carolina, United States Blood-based biomarkers show promise as a noninvasive method for measuring Alzheimer’s disease pathology and neurodegeneration throughout the lifecourse. However, the relationship between longitudinal changes in these biomarkers and late-life brain morphology in community-dwelling populations requires further investigation. Between 2011 and 2013, 1,977 participants from the Atherosclerosis Risk in Communities Study received underwent 3 Tesla magnetic resonance imaging scans. Whole-brain cortical thickness was quantified by Freesurfer. Stored plasma samples collected in midlife (1993-95, mean age 59.0 years) and late-life (2011-13, mean age 76.8 years) from asubsample of 1,515 participants (60.7% female, 25.5% Black adults) were assayed in 2022 using Quanterix SiMoA. The assay quantified amyloid-β (Aβ)42/40, phosphorylated tau at threonine 181 (p-Tau181), neurofilament light (NfL), and glial fibrillary acidic protein (GFAP) . Linear regression models estimated the association of blood-based biomarkers from midlife, late-life, and the change from midlife to late-life with cortical thickness in late-life. In models adjusted for demographics, lifestyle factors, cardiovascular factors, and the presence of APOE ε4 alleles, higher midlife measures of p-Tau181 and increases from midlife to late-life in NfL and GFAP were associated with lower cortical thickness in late-life. Concurrent measures of p-Tau181, NfL, and GFAP were associated with lower cortical thickness in late-life and exhibited a stronger association among participants ≥75 years old compared to participants <75 years old. Additional longitudinal research is needed to determine whether blood-based biomarkers predict cortical thinning over time and may serve asan early indicator of accelerated brain atrophy.

FAQs

What was the main goal of the study?

To determine how changes in blood-based biomarkers of Alzheimer’s disease relate to late-life cortical thickness in community-dwelling populations.

How were cortical thickness and biomarkers measured?

Cortical thickness was quantified from 3T MRI using FreeSurfer, and midlife and late-life plasma samples were assayed in 2022 with Quanterix SiMoA for Aβ42/40, p-Tau181, NfL, and GFAP.

Which biomarker changes were linked to cortical thinning in late life?

Higher midlife p-Tau181 and increases from midlife to late-life in NfL and GFAP were associated with lower cortical thickness in late life.

Sep 28, 2026

Upload by Maya Linwood