title: Cognitive and anatomic contributions of metabolic decline in Alzheimer disease and cerebrovascular disease.
abstract: BACKGROUND
  Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline. Understanding how each disease contributes to dementia is essential from both a pathophysiologic and diagnostic perspective.
  
  
  OBJECTIVE
  To elucidate how baseline cognitive function (episodic memory and executive function) and brain anatomy (white matter hyperintensities and hippocampal volume) are associated with baseline (positron emission tomography-1 [PET1]) and longitudinal (PET2) glucose metabolism in 38 subjects older than 55 years ranging from normal cognition, cognitive impairment without dementia, and dementia.
  
  
  METHODS
  Cross-sectional regression analyses across subjects.
  
  
  METHODS
  Multicenter, university-based study of subcortical vascular dementia.
  
  
  METHODS
  Regional cerebral glucose metabolism was the primary outcome, with the major hypotheses that memory and hippocampal volume are related to temporoparietal hypometabolism while executive function and white matter hyperintensities correlate with frontal lobe hypometabolism.
  
  
  RESULTS
  Low baseline hippocampal volume predicted longitudinal development (PET2) of medial temporal hypometabolism. Lower memory was associated with parietal and cingulate hypometabolism at PET1, which increased at the 2-year-follow-up (PET2). Executive function was associated with frontal and temporoparietal hypometabolism at PET1 but only with frontal hypometabolism at follow-up. White matter hyperintensities predicted hypometabolism over time in the frontoparietal regions, predicting a rate of metabolic change (PET1 - PET2/time).
  
  
  CONCLUSIONS
  Low baseline episodic memory and hippocampal volume predict the metabolic alterations associated with Alzheimer disease, whereas elevated baseline white matter hyperintensities predict a different pattern of metabolic decline that is plausibly associated with cerebrovascular disease.
authors.affiliation: Helen Wills Neuroscience Institute and the Lawrence Berkeley National Laboratory, University of California, Berkeley, CA 94720, USA. beth.kuczynski@gmail.com
authors.forename: Beth
authors.initials: B
authors.lastname: Kuczynski
authors.forename: Bruce
authors.initials: B
authors.lastname: Reed
authors.forename: Dan
authors.initials: D
authors.lastname: Mungas
authors.forename: Michael
authors.initials: M
authors.lastname: Weiner
authors.forename: Helena C
authors.initials: HC
authors.lastname: Chui
authors.forename: William
authors.initials: W
authors.lastname: Jagust
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology*; D001284:Atrophy / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology*; D001928:Brain Diseases, Metabolic / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D001931:Brain Mapping; D003072:Cognition Disorders / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D003430:Cross-Sectional Studies; D015140:Dementia, Vascular / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology*; D018450:Disease Progression; D004734:Energy Metabolism / Q000502:physiology; D005260:Female; D005947:Glucose / Q000378:metabolism; D006624:Hippocampus / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008297:Male; D008569:Memory Disorders / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D009413:Nerve Fibers, Myelinated / Q000378:metabolism / Q000473:pathology; D009483:Neuropsychological Tests; D049268:Positron-Emission Tomography; D011237:Predictive Value of Tests
chemical_list: D005947:Glucose