Black individuals showed an accelerated pattern of brain aging beginning in midlife, a cross-sectional analysis of two community-based cohorts showed.
According to Adam Brickman, Ph.D., of Columbia University in New York City, and colleagues, the association between age and cortical thickness and white matter hyperintensity (WMH) volume was more significant in late life than midlife for latinos and white participants but not for black people.
Researchers found that the amount of brain ageing in black participants was identical in both midlife and later age; the study was published in JAMA Neurology.
“We postulate that race and ethnicity disparities in brain aging are due to lifetime cumulative exposure to structural and social forces that elevate subsequent exposure to risk factors for brain pathology,” Brickman and co-authors wrote.
However, no research have evaluated brain health at midlife versus later life relative to white adults, they noted. Previous studies have shown that racial and ethnic minorities have worse brain health in late life.
The Washington Heights Inwood Columbia Aging Project (WHICAP) late-life cohort of 970 participants and the Offspring Study of Racial and Ethnic Disparities in Alzheimer Disease (Offspring) midlife cohort of 497 participants underwent MRI assessments to detect cerebrovascular disease and neurodegeneration.
The WHICAP late-life cohort of 970 participants and 497 of their adult children who participated in the Offspring midlife cohort underwent MRI assessments to detect cerebrovascular disease and neurodegeneration.
About 35% of WHICAP participants were Black, 40% were Latinos, and 25% were White, with a mean age of about 75. The participants in Offspring were 55 years old on average, 24% of them were Black, 70% were Latinos, and 6.4% were White. Both cohorts included about 65% female members. Participants disclosed any history of diabetes, hypertension, heart disease, and clinical stroke at the time of the MRI scan. WMH volume and cortical thickness were outcomes.
In comparison to prior findings, Black-White disparities were often greater than Latino-White differences for both measures, whereas Black-Latino disparities were negligible. Both midlife (Black-white B=0.357, P=0.046) and late life (Black-Latino B=0.149, P0.001; Black-white B=0.166, P0.001) saw WMH discrepancies. Only in late life were cortical thickness differences visible (Black-Latino B=-0.037, P 0.001; Black-White B=-0.064, P 0.001). For Latinos (cortical thickness B=0.006, P.001; WMH volume B=-0.010, P=0.03) and White (cortical thickness B=0.005, P=0.001; WMH volume B=-0.021, P=0.07) subjects, brain ageing was more pronounced in late life compared to midlife. This was not the case for Black participants, who revealed comparable robust relationships between age and MRI measurements in midlife and late life (cortical thickness B=0.001,?P=0.64; WMH volume B=0.003,?P=0.61).
The findings have clear implications for cognitive ageing, the team stated, and white matter hyperintensities and cortical thicknesses are well-known predictors or indicators of cognitive health, including in the current study. The size of racial and ethnic variations in WMH volume may have been greater in midlife compared to late life due to varying survival rates between racial and ethnic groups, the researchers cautioned.
The study’s cross-sectional methodology and possible restricted generalizability due to the middle-aged group’s lower number of white participants compared to the older cohort were limitations.
In order to ascertain whether these forces influence observed differences in brain health, their functional ramifications, and secular trends across time, future studies should take into account measurement of these forces across the life course, according to Brickman and colleagues. To elucidate the causes of differences in brain ageing and Alzheimer’s disease, they noted that pathological biomarkers like amyloid and tau should be included in future research.