title: Coronary artery calcium, brain function and structure: the AGES-Reykjavik Study.
abstract: OBJECTIVE
  Several cardiovascular risk factors are associated with cognitive disorders in older persons. Little is known about the association of the burden of coronary atherosclerosis with brain structure and function.
  
  
  METHODS
  This is a cross-sectional analysis of data from the Age, Gene, Environment Susceptibility (AGES)-Reykjavik Study cohort of men and women born 1907 to 1935. Coronary artery calcification (CAC), a marker of atherosclerotic burden, was measured with CT. Memory, speed of processing, and executive function composites were calculated from a cognitive test battery. Dementia was assessed in a multistep procedure and diagnosed according to international guidelines. Quantitative data on total intracranial and tissue volumes (total, gray matter volume, white matter volume, and white matter lesion volume), cerebral infarcts, and cerebral microbleeds were obtained with brain MRI. The association of CAC with dementia (n=165 cases) and cognitive function in nondemented subjects (n=4085), and separately with MRI outcomes, was examined in multivariate models adjusting for demographic and vascular risk factors. Analyses tested whether brain structure mediated the associations of CAC to cognitive function.
  
  
  RESULTS
  Subjects with higher CAC were more likely to have dementia and lower cognitive scores, more likely to have lower white matter volume, gray matter volume, and total brain tissue, and to have more cerebral infarcts, cerebral microbleeds, and white matter lesions. The relations of cognitive performance and dementia to CAC were significantly attenuated when the models were adjusted for brain lesions and volumes.
  
  
  CONCLUSIONS
  In a population-based sample, increasing atherosclerotic load assessed by CAC is associated with poorer cognitive performance and dementia, and these relations are mediated by evidence of brain pathology.
authors.affiliation: National Institutes of Health, NIA/LEDB, 7201 Wisconsin Ave, Gateway Building, Suite 3C309, Bethesda, MD 20892-9205, USA.
authors.forename: Jean-Sébastien
authors.initials: JS
authors.lastname: Vidal
authors.forename: Sigurdur
authors.initials: S
authors.lastname: Sigurdsson
authors.forename: Maria K
authors.initials: MK
authors.lastname: Jonsdottir
authors.forename: Gudny
authors.initials: G
authors.lastname: Eiriksdottir
authors.forename: Gudmundur
authors.initials: G
authors.lastname: Thorgeirsson
authors.forename: Olafur
authors.initials: O
authors.lastname: Kjartansson
authors.forename: Melissa E
authors.initials: ME
authors.lastname: Garcia
authors.forename: Mark A
authors.initials: MA
authors.lastname: van Buchem
authors.forename: Tamara B
authors.initials: TB
authors.lastname: Harris
authors.forename: Vilmundur
authors.initials: V
authors.lastname: Gudnason
authors.forename: Lenore J
authors.initials: LJ
authors.lastname: Launer
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000235:genetics / Q000473:pathology / Q000502:physiology*; D001921:Brain / Q000473:pathology / Q000502:physiology*; D002114:Calcinosis / Q000453:epidemiology* / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D003072:Cognition Disorders / Q000453:epidemiology / Q000235:genetics / Q000473:pathology; D015331:Cohort Studies; D003324:Coronary Artery Disease / Q000453:epidemiology* / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D003331:Coronary Vessels / Q000473:pathology / Q000502:physiology*; D003430:Cross-Sectional Studies; D004777:Environment; D005260:Female; D020022:Genetic Predisposition to Disease / Q000453:epidemiology* / Q000235:genetics; D006801:Humans; D007055:Iceland / Q000453:epidemiology; D008279:Magnetic Resonance Imaging; D008297:Male