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Brain Aging Among Racially and Ethnically Diverse Middle-Aged and Older Adults

Abstract

Importance: Neuroimaging studies have documented racial and ethnic disparities in brain health in old age. It remains unclear whether these disparities are apparent in midlife.

Objective: To assess racial and ethnic disparities in magnetic resonance imaging (MRI) markers of cerebrovascular disease and neurodegeneration in midlife and late life.

Design, Setting, And Participants: Data from 2 community-based cohort studies, Washington Heights-Inwood Columbia Aging Project (WHICAP) and the Offspring Study of Racial and Ethnic Disparities in Alzheimer Disease (Offspring), were used. Enrollment took place from March 2011 and June 2017, in WHICAP and Offspring, respectively, to January 2021. Of the 822 Offspring and 1254 WHICAP participants approached for MRI scanning, 285 and 176 refused participation in MRI scanning, 36 and 76 were excluded for contraindications/ineligibility, and 4 and 32 were excluded for missing key variables, respectively.

Main Outcomes And Measures: Cortical thickness in Alzheimer disease-related regions, white matter hyperintensity (WMH) volume.

Results: The final sample included 1467 participants. Offspring participants (497 [33.9%]) had a mean (SD) age of 55 (10.7) years, had a mean (SD) of 13 (3.5) years of education, and included 117 Black individuals (23.5%), 348 Latinx individuals (70%), 32 White individuals (6.4%), and 324 women (65.2%). WHICAP participants (970 [66.1%]) had a mean (SD) age of 75 (6.5) years, had a mean (SD) of 12 (4.7) years of education, and included 338 Black individuals (34.8%), 389 Latinx individuals (40.1%), 243 White individuals (25.1%), and 589 women (65.2%). Racial and ethnic disparities in cerebrovascular disease were observed in both midlife (Black-White: B = 0.357; 95% CI, 0.708-0.007; P = .046) and late life (Black-Latinx: B = 0.149, 95% CI, 0.068-0.231; P < .001; Black-White: B = 0.166; 95% CI, 0.254-0.077; P < .001), while disparities in cortical thickness were evident in late life only (Black-Latinx: B = -0.037; 95% CI, -0.055 to -0.019; P < .001; Black-White: B = -0.064; 95% CI -0.044 to -0.084; P < .001). Overall, Black-White disparities were larger than Latinx-White disparities for cortical thickness and WMH volume. Brain aging, or the association of age with MRI measures, was greater in late life compared with midlife for Latinx (cortical thickness: B = 0.006; 95% CI, 0.004-0.008; P < .001; WMH volume: B = -0.010; 95% CI, -0.018 to -0.001; P = .03) and White (cortical thickness: B = 0.005; 95% CI, 0.002-0.008; P = .001; WMH volume: B = -0.021; 95% CI -0.043 to 0.002; P = .07) participants but not Black participants (cortical thickness: B = 0.001; 95% CI, -0.002 to 0.004; P =.64; WMH volume: B = 0.003; 95% CI, -0.010 to 0.017; P = .61), who evidenced a similarly strong association between age and MRI measures in midlife and late life.

Conclusions And Relevance: In this study, racial and ethnic disparities in small vessel cerebrovascular disease were apparent in midlife. In Latinx and White adults, brain aging was more pronounced in late life than midlife, whereas Black adults showed accelerated pattern of brain aging beginning in midlife.

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References
1.
Walker K, Power M, Hoogeveen R, Folsom A, Ballantyne C, Knopman D . Midlife Systemic Inflammation, Late-Life White Matter Integrity, and Cerebral Small Vessel Disease: The Atherosclerosis Risk in Communities Study. Stroke. 2017; 48(12):3196-3202. PMC: 5705320. DOI: 10.1161/STROKEAHA.117.018675. View

2.
Amieva H, Le Goff M, Millet X, Orgogozo J, Peres K, Barberger-Gateau P . Prodromal Alzheimer's disease: successive emergence of the clinical symptoms. Ann Neurol. 2008; 64(5):492-8. DOI: 10.1002/ana.21509. View

3.
Brickman A, Provenzano F, Muraskin J, Manly J, Blum S, Apa Z . Regional white matter hyperintensity volume, not hippocampal atrophy, predicts incident Alzheimer disease in the community. Arch Neurol. 2012; 69(12):1621-7. PMC: 3597387. DOI: 10.1001/archneurol.2012.1527. View

4.
Manly J, Jacobs D, Sano M, Bell K, Merchant C, Small S . Cognitive test performance among nondemented elderly African Americans and whites. Neurology. 1998; 50(5):1238-45. DOI: 10.1212/wnl.50.5.1238. View

5.
Glymour M, Weuve J, Chen J . Methodological challenges in causal research on racial and ethnic patterns of cognitive trajectories: measurement, selection, and bias. Neuropsychol Rev. 2008; 18(3):194-213. PMC: 3640811. DOI: 10.1007/s11065-008-9066-x. View