Brain volume decline in aging: evidence for a relation between socioeconomic status, preclinical Alzheimer disease, and reserve.

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.

[1]  D. A. Pond,et al.  Social Class and Mental Illness , 1958, Mental Health.

[2]  R. G. Hunt,et al.  Social Class and Mental Illness , 1959 .

[3]  Daniel H. Mathalon,et al.  Correction for head size in brain-imaging measurements , 1993, Psychiatry Research: Neuroimaging.

[4]  J M Lepkowski,et al.  The social stratification of aging and health. , 1994, Journal of health and social behavior.

[5]  N. Volkow,et al.  Distribution Volume Ratios without Blood Sampling from Graphical Analysis of PET Data , 1996, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[6]  J. Price,et al.  Clinicopathologic studies in cognitively healthy aging and Alzheimer's disease: relation of histologic markers to dementia severity, age, sex, and apolipoprotein E genotype. , 1998, Archives of neurology.

[7]  L. Fratiglioni,et al.  The effect of education on dementia occurrence in an Italian population with middle to high socioeconomic status , 1998, Neurology.

[8]  Nick C Fox,et al.  Serial magnetic resonance imaging of cerebral atrophy in preclinical Alzheimer's disease , 1999, The Lancet.

[9]  Laura Fratiglioni,et al.  Worldwide Prevalence and Incidence of Dementia , 1999, Drugs & aging.

[10]  Alan C. Evans,et al.  Brain development during childhood and adolescence: a longitudinal MRI study , 1999, Nature Neuroscience.

[11]  G. Ratcliff,et al.  Relation of education to brain size in normal aging , 1999, Neurology.

[12]  W R Markesbery,et al.  Linguistic Ability in Early Life and the Neuropathology of Alzheimer's Disease and Cerebrovascular Disease: Findings from the Nun Study , 2000, Annals of the New York Academy of Sciences.

[13]  Donald H. Lee,et al.  Relationships between factors of intelligence and brain volume , 2000 .

[14]  J. Price,et al.  Absence of cognitive impairment or decline in preclinical Alzheimer’s disease , 2001, Neurology.

[15]  M. D'Andrea,et al.  Lipofuscin and Aβ42 exhibit distinct distribution patterns in normal and Alzheimer's disease brains , 2002, Neuroscience Letters.

[16]  W. Klunk,et al.  Synthesis and evaluation of 11C-labeled 6-substituted 2-arylbenzothiazoles as amyloid imaging agents. , 2003, Journal of medicinal chemistry.

[17]  J. Schneider,et al.  Education modifies the relation of AD pathology to level of cognitive function in older persons , 2003, Neurology.

[18]  W. Klunk,et al.  Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound‐B , 2004, Annals of neurology.

[19]  R. Buckner Memory and Executive Function in Aging and AD Multiple Factors that Cause Decline and Reserve Factors that Compensate , 2004, Neuron.

[20]  Abraham Z. Snyder,et al.  A unified approach for morphometric and functional data analysis in young, old, and demented adults using automated atlas-based head size normalization: reliability and validation against manual measurement of total intracranial volume , 2004, NeuroImage.

[21]  C. Van Petten,et al.  Relationship between hippocampal volume and memory ability in healthy individuals across the lifespan: review and meta-analysis. , 2004, Neuropsychologia.

[22]  T. Fritsch,et al.  Worker functions and traits associated with occupations and the development of AD , 2004, Neurology.

[23]  C. Jack,et al.  Comparison of different MRI brain atrophy rate measures with clinical disease progression in AD , 2004, Neurology.

[24]  R. Sapolsky Social Status and Health in Humans and Other Animals , 2004 .

[25]  Benjamin J. Shannon,et al.  Molecular, Structural, and Functional Characterization of Alzheimer's Disease: Evidence for a Relationship between Default Activity, Amyloid, and Memory , 2005, The Journal of Neuroscience.

[26]  J. Morris,et al.  Predictors of preclinical Alzheimer disease and dementia: a clinicopathologic study. , 2005, Archives of neurology.

[27]  Jean-François Dartigues,et al.  The 9 year cognitive decline before dementia of the Alzheimer type: a prospective population-based study. , 2005, Brain : a journal of neurology.

[28]  Cheryl L. Dahle,et al.  Regional brain changes in aging healthy adults: general trends, individual differences and modifiers. , 2005, Cerebral cortex.

[29]  R. Buckner,et al.  Normative estimates of cross-sectional and longitudinal brain volume decline in aging and AD , 2005, Neurology.

[30]  P. Sachdev,et al.  Brain reserve and dementia: a systematic review , 2005, Psychological Medicine.

[31]  Paul Edison,et al.  Amyloid load and cerebral atrophy in Alzheimer's disease: An 11C‐PIB positron emission tomography study , 2006, Annals of neurology.

[32]  J Philip Miller,et al.  Longitudinal course and neuropathologic outcomes in original vs revised MCI and in pre-MCI , 2006, Neurology.

[33]  Y. Stern Cognitive Reserve and Alzheimer Disease , 2006, Alzheimer disease and associated disorders.

[34]  Yvette I. Sheline,et al.  Potential antecedent marker of Alzheimer disease , 2006 .

[35]  Y. Stern,et al.  Education and rates of cognitive decline in incident Alzheimer’s disease , 2005, Journal of Neurology, Neurosurgery & Psychiatry.

[36]  Gina N. LaRossa,et al.  Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Aβ42 in humans , 2006, Annals of neurology.