Brain Volume Decline in Aging: Evidence for a Relation Between Socioeconomic Status, Preclinical Alzheimer Disease, and Reserve | Dementia and Cognitive Impairment | JAMA Neurology | JAMA Network
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Original Contribution
January 2008

Brain Volume Decline in Aging: Evidence for a Relation Between Socioeconomic Status, Preclinical Alzheimer Disease, and Reserve

Author Affiliations

Author Affiliations: Division of Biology and Biomedical Sciences (Mr Fotenos and Dr Buckner), Mallinckrodt Institute of Radiology (Drs Mintun and Snyder), and Department of Neurology (Drs Snyder and Morris), Washington University Medical School, St Louis, Missouri; Department of Psychology, Center for Brain Science, Howard Hughes Medical Institute, Harvard University, Cambridge, Massachusetts (Dr Buckner); and Martinos Center, Massachusetts General Hospital, Department of Radiology, Harvard Medical School, Boston (Dr Buckner).

Arch Neurol. 2008;65(1):113-120. doi:10.1001/archneurol.2007.27

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 (11C).

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 × 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.