Baseline levels and longitudinal rates of change in plasma Aβ42/40 among self-identified Black/African American and White individuals

Abstract

Abstract Objective: The use of blood-based biomarkers of Alzheimer disease (AD) may facilitate access to biomarker testing of groups that have been historically under-represented in research. We evaluated whether plasma Aβ42/40 has similar or different baseline levels and longitudinal rates of change in participants racialized as Black or White. Methods: The Study of Race to Understand Alzheimer Biomarkers (SORTOUT-AB) is a multi-center longitudinal study to evaluate for potential differences in AD biomarkers between individuals racialized as Black or White. Plasma samples collected at three AD Research Centers (Washington University, University of Pennsylvania, and University of Alabama-Birmingham) underwent analysis with C2N Diagnostics’ PrecivityAD™ blood test for Aβ42 and Aβ40. General linear mixed effects models were used to estimate the baseline levels and rates of longitudinal change for plasma Aβ measures in both racial groups. Analyses also examined whether dementia status, age, sex, education, APOE ε4 carrier status, medical comorbidities, or fasting status modified potential racial differences. Results: Of the 324 Black and 1,547 White participants, there were 158 Black and 759 White participants with plasma Aβ measures from at least two longitudinal samples over a mean interval of 6.62 years. At baseline, the group of Black participants had lower levels of plasma Aβ40 but similar levels of plasma Aβ42 as compared to the group of White participants. As a result, baseline plasma Aβ42/40 levels were higher in the Black group than the White group, consistent with the Black group having lower levels of amyloid pathology. Racial differences in plasma Aβ42/40 were not modified by age, sex, education, APOE ε4 carrier status, medical conditions (hypertension and diabetes), or fasting status. Despite differences in baseline levels, the Black and White groups had a similar longitudinal rate of change in plasma Aβ42/40. Interpretation: Black individuals participating in AD research studies had a higher mean level of plasma Aβ42/40, consistent with a lower level of amyloid pathology, which, if confirmed, may imply a lower proportion of Black individuals being eligible for AD clinical trials in which the presence of amyloid is a prerequisite. However, there was no significant racial difference in the rate of change in plasma Aβ42/40, suggesting that amyloid pathology accumulates similarly across racialized groups.