Racial differences in Alzheimer biomarkers among early‐stage symptomatic and cognitively normal Alzheimer Disease Research Center (ADRC) participants

Abstract

AbstractBackgroundThere are few assessments of possible racial differences in Alzheimer disease (AD) biomarkers because research cohorts typically are not diverse. Should differences exist, they may inform the understanding of AD pathogenesis as well as the role of social determinants of health (SDOH).MethodWe assessed a non‐clinic‐based cohort of 1255 community living persons, age 45 and older, who were enrolled in studies of aging and dementia at the Knight ADRC (St Louis, Missouri, USA). Participants completed at least one brain magnetic resonance imaging (MRI) study, and/or at least one amyloid positron emission tomography (PET) scan, and/or at least one lumbar puncture to obtain cerebrospinal fluid (CSF) for biomarker assays. The cohort included 1082 white participants and 173 participants who self‐identified as Black or African American (AA); 33% of participants in each group had early‐stage symptomatic AD and 67% in each group were cognitively normal.ResultBoth racial groups demonstrated expected biomarker changes as a function of clinical status (eg, lower hippocampal volumes in persons with symptomatic AD). Higher body mass index and HgA1c levels were noted in AAs, but there was no racial difference in the frequency of MRI‐confirmed cerebral infarcts. There also were no differences in the mean cortical standardized uptake value ratios for Pittsburgh Compound B or in amyloid‐beta42 concentrations in CSF. However, mean CSF concentrations of tau and phosphorylated tau181 were lower in AA participants, a finding that was evident primarily in carriers of the ε4 allele of APOE. The CSF concentrations of soluble TREM2, a mediator of the inflammatory response to AD pathology, also were lower in AAs. Finally, decreased volumes in brain regions comprising the AD cortical signature were lower in AAs but this difference was mediated, at least in part, by SDOH.ConclusionThere are racial differences in AD biomarkers between white and AA research participants, including for the AD cortical signature, a putative marker of neurodegeneration in the AT(N) framework. SDOH contribute to these differences, either independently or through interactions with biological factors.