title: Longitudinal volumetric MRI change and rate of cognitive decline.
abstract: OBJECTIVE
  To examine how baseline and change of volumetric MRI relate to cognitive decline in older individuals.
  
  
  BACKGROUND
  Memory is associated with hippocampal integrity, whereas executive function has been linked to impaired frontal lobe function. Previous studies have shown that hippocampal and cortical atrophy are more strongly related to cognition than are measures of subcortical cerebrovascular disease (CVD). The authors hypothesized that memory (MEM) decline would be related to change in hippocampal volume (HC), whereas decline in executive function (EXEC) would be related to change of cortical gray matter volume (CGM) and measures of subcortical CVD.
  
  
  METHODS
  Subjects from a multicenter study (n = 103) included cognitively normal, mildly impaired, and demented cases with and without subcortical lacunes. All had longitudinal cognitive evaluation (mean = 4.8 years) and two or more MRI scans at least one year apart (mean = 3.4 years). MRI measures included HC, CGM, total lacune volume (LAC), and white matter hyperintensity volume (WMH). Random effects modeling of longitudinal data assessed effects of MRI baseline and MRI change on baseline and change of psychometrically matched measures of MEM and EXEC.
  
  
  RESULTS
  Change in MEM was related to HC baseline and HC change. Change in EXEC was related to baseline CGM and to change in CGM, HC, and LAC. Results were unchanged when demented cases were excluded. WMH was not associated with change in MEM or EXEC independent of HC, CGM, and LAC.
  
  
  CONCLUSIONS
  Hippocampal volume was the primary determinant of memory decline, whereas executive function (EXEC) decline was related to multiple brain components. Results support a hypothesis that MEM decline is strongly influenced by Alzheimer disease (AD), whereas EXEC decline may be complexly determined by cerebrovascular disease and AD.
authors.affiliation: Department of Neurology, School of Medicine, University of California, Davis, Sacramento, CA 95817, USA. dmmungas@ucdavis.edu
authors.forename: D
authors.initials: D
authors.lastname: Mungas
authors.forename: D
authors.initials: D
authors.lastname: Harvey
authors.forename: B R
authors.initials: BR
authors.lastname: Reed
authors.forename: W J
authors.initials: WJ
authors.lastname: Jagust
authors.forename: C
authors.initials: C
authors.lastname: DeCarli
authors.forename: L
authors.initials: L
authors.lastname: Beckett
authors.forename: W J
authors.initials: WJ
authors.lastname: Mack
authors.forename: J H
authors.initials: JH
authors.lastname: Kramer
authors.forename: M W
authors.initials: MW
authors.lastname: Weiner
authors.forename: N
authors.initials: N
authors.lastname: Schuff
authors.forename: H C
authors.initials: HC
authors.lastname: Chui
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000375:Aging / Q000473:pathology*; D000544:Alzheimer Disease / Q000175:diagnosis / Q000503:physiopathology / Q000523:psychology; D001284:Atrophy / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D001921:Brain / Q000473:pathology* / Q000503:physiopathology; D002540:Cerebral Cortex / Q000473:pathology / Q000503:physiopathology; D003072:Cognition Disorders / Q000175:diagnosis* / Q000503:physiopathology / Q000523:psychology; D003625:Data Collection; D003704:Dementia / Q000175:diagnosis / Q000503:physiopathology; D015140:Dementia, Vascular / Q000175:diagnosis / Q000503:physiopathology / Q000523:psychology; D018450:Disease Progression; D005260:Female; D006624:Hippocampus / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D008137:Longitudinal Studies; D008279:Magnetic Resonance Imaging; D008297:Male; D008569:Memory Disorders / Q000175:diagnosis* / Q000503:physiopathology / Q000523:psychology; D008875:Middle Aged; D009483:Neuropsychological Tests; D011237:Predictive Value of Tests