Blood‐based biomarkers for neurodegeneration in non‐Hispanic Black and White older adults: Results from the Einstein Aging Study (EAS)

Abstract

AbstractBackgroundWith recent technological advancements, neurodegenerative biomarkers (NDBMs) in blood plasma now produce results comparable to those obtained in cerebrospinal fluid, supporting the possibility of less invasive and costly determination of risk status for Alzheimer’s disease (AD). However, most research with these novel biomarkers has been in predominately non‐Hispanic (NH) White samples. Hence, little is known about distributions of these biomarkers among NH Blacks despite their elevated risk for AD.MethodBlood plasma samples were obtained from 254 older participants in the EAS who were free of dementia (mean age [SD]=77.6[4.9] years; range 70‐93 years; 66.1% female; 46.5% NH Black, 53.5% NH White; 27.2% mild cognitive impairment (MCI) as defined by Jak/Bondi criteria). AD biomarkers [β‐amyloid (Aβ40, Aβ42), pTau181], along with biomarkers of generalized neuronal damage and astrocyte activation [neurofilament light (NfL) and glial fibrillary acidic protein (GFAP), respectively] were quantified in blood using Single molecule array (Simoa) assays on HD‐X Analyzers (Quanterix, Billerica, MA). Comparisons of NDBMs between groups were conducted using Wilcoxon rank sum test in unadjusted analyses, and linear regression models adjusting for covariates including age, gender, education, diabetes history, myocardial infarction, and hypertension.ResultWe observed lower overall levels of NDBMs in NH Blacks vs. NH Whites regardless of MCI status (Aβ40, Aβ42, and NfL (ps<0.05) see Table 1). Among NH Whites, those with MCI had higher Aβ40, Aβ42, and NfL (ps<0.05) compared to cognitively normal individuals; no significant differences by MCI status were observed among NH Blacks (not shown). The above race differences in Aβ40, Aβ42, and NfL remained evident across the full sample in linear regression analyses (adjusted for MCI status and covariates). When stratified by MCI status, race differences remained evident for NfL (regardless of MCI status); for Aβ40, race differences were evident among individuals with MCI only (see Table 2). Although individual analytes differed, the Aβ42/Aβ40 ratio did not differ by race.ConclusionNH Blacks exhibited lower overall levels of NDBMs compared to NH Whites, and associations between NDBMs and MCI were in the expected directions only among NH Whites. These race differences suggest that future work is needed to develop generalizable norms for blood‐based NDBMs.