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.
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.
Authors: Reisa A Sperling; Paul S Aisen; Laurel A Beckett; David A Bennett; Suzanne Craft; Anne M Fagan; Takeshi Iwatsubo; Clifford R Jack; Jeffrey Kaye; Thomas J Montine; Denise C Park; Eric M Reiman; Christopher C Rowe; Eric Siemers; Yaakov Stern; Kristine Yaffe; Maria C Carrillo; Bill Thies; Marcelle Morrison-Bogorad; Molly V Wagster; Creighton H Phelps Journal: Alzheimers Dement Date: 2011-04-21 Impact factor: 21.566
Authors: Richard P Kline; Elizabeth Pirraglia; Hao Cheng; Susan De Santi; Yi Li; Michael Haile; Mony J de Leon; Alex Bekker Journal: Anesthesiology Date: 2012-03 Impact factor: 7.892
Authors: Anders M Fjell; Lars T Westlye; Thomas Espeseth; Ivar Reinvang; Anders M Dale; Dominic Holland; Kristine B Walhovd Journal: Neuropsychology Date: 2010-03 Impact factor: 3.295
Authors: D F Tate; E S Neeley; M C Norton; J T Tschanz; M J Miller; L Wolfson; C Hulette; C Leslie; K A Welsh-Bohmer; B Plassman; Erin D Bigler Journal: Brain Res Date: 2010-12-21 Impact factor: 3.252
Authors: Maria C Norton; Ken R Smith; Truls Østbye; JoAnn T Tschanz; Chris Corcoran; Sarah Schwartz; Kathleen W Piercy; Peter V Rabins; David C Steffens; Ingmar Skoog; John C S Breitner; Kathleen A Welsh-Bohmer Journal: J Am Geriatr Soc Date: 2010-05 Impact factor: 5.562