Objectives: To assess the relation between socioeconomic status (SES) and structural brain change in nondemented older adults and to ascertain the potential role of preclinical Alzheimer disease (AD).
Design: Cross-sectional and longitudinal observation.
Setting: Alzheimer's Disease Research Center, St Louis, Missouri.
Participants: Volunteer sample of 362 nondemented adults aged 18 to 93 years. The main cohort of 100 was evaluated for dementia and SES; a Clinical Dementia Rating (CDR) of 0 (no dementia) and middle, high-middle, or high SES was required for eligibility. All 362 received magnetic resonance imaging; of the main 100, 91 received follow-up clinical assessment, and 33 received follow-up magnetic resonance imaging over at least a 3-year interval. A separate sample of 58 CDR 0 participants (aged 47 to 86 years) took part in amyloid imaging with Pittsburgh Compound B (PiB) labeled with radioactive carbon ((11)C).
Main outcome measures: Whole-brain volume adjusted for head size (aWBV) and change per year.
Results: aWBV declined by 0.22% per year between the ages of 20 and 80 years with accelerated decline in advanced aging. Controlling for effects of age and sex in older adults (>65 years) with CDR 0, higher SES was associated with smaller aWBV (3.8% difference spanning the sample range from middle to high privilege, P< .01) and more rapid volume loss (0.39% per year to 0.68% per year from middle to high privilege, P< .05). aWBV was reduced by 2.5% in individuals positive for PiB binding (n=9) as compared with individuals negative for PiB binding (n=49, P< .05), supporting an influence of undetected preclinical AD. Follow-up clinical data revealed that brain volume reduction associated with SES was greater in those who later developed very mild dementia (preclinical CDR 0 group, n=19) compared with those who remained nondemented (stable CDR 0 group, n=64; group x SES interaction, P< .05).
Conclusions: Privileged nondemented older adults harbor more preclinical brain atrophy, consistent with their having greater reserve against the expression of AD.