Abstract

AbstractBackgroundSubjective cognitive decline (SCD) may represent an early clinical manifestation of Alzheimer’s disease (AD) pathology. There is evidence of an association between amyloid deposition and SCD. Given disparities in risk of AD and cognitive impairment across ethnoracial groups, there is need to evaluate SCD, cognition, and markers of AD across diverse samples, as well as study partners as reporters of SCD.MethodParticipants included 267 non‐Hispanic Black, 5241 non‐Hispanic White, 225 Hispanic White, and 228 Asian individuals who presented for screening for the Anti‐Amyloid in Asymptomatic Alzheimer’s Disease (A4) study (N = 5961). Participants completed the Preclinical Alzheimer Cognitive Composite (PACC) and self‐ and study partner‐report of SCD (Cognitive Function Instrument/CFI). A subsample of participants underwent amyloid PET (N = 4416). In a series of within‐group linear regressions, we evaluated the relationships between 1) self‐reported SCD and cognitive performance 2) study partner‐ and self‐reported SCD, and 3) participant amyloid status and SCD.ResultAsian participants self‐reported the highest SCD and non‐Hispanic White participants reported the lowest. Controlling for age, education, and gender, PACC performance was significantly associated with self‐reported SCD in non‐Hispanic White (R2 = 0.039, b = ‐0.141, p < .0001), non‐Hispanic Black (R2 = 0.055, b = ‐0.158, p < .01), and Asian samples (R2 = 0.093, b = ‐0.318, p < .0001), with better PACC performance associated with lower CFI. PACC was not significantly associated with CFI in the Hispanic sample (R2 = .003, b = ‐0.097, p = .0636). Self‐ and study partner report of SCD were significantly correlated in all groups. Amyloid burden was associated with greater self‐reported SCD in non‐Hispanic White (R2 = 0.018, b = 0.452, p < .001) and Asian samples (R2 = 0.046, b = 1.58, p < .01), but not in the non‐Hispanic Black (R2 = 0.020, b = ‐.501, p = .277) and Hispanic participants (R2 = 0.016, b = 0.638, p = .169).ConclusionSCD appears similarly related to cognitive performance across most groups, and there is alignment between self‐ and study‐partner report of SCD across groups. There is evidence of variability in the association between AD biomarkers and SCD across racial groups, albeit in a smaller subsample with PET imaging. Future work should evaluate sociocultural factors that may contribute to differences in the value of SCD in individuals at risk for symptomatic AD.

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