Cognitive and Anatomic Contributions of Metabolic Decline in Alzheimer Disease and Cerebrovascular Disease

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...

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Published inArchives of neurology (Chicago) Vol. 65; no. 5; pp. 650 - 655
Main Authors Kuczynski, Beth, Reed, Bruce, Mungas, Dan, Weiner, Michael, Chui, Helena C, Jagust, William
Format Journal Article
LanguageEnglish
Published Chicago, IL American Medical Association 01.05.2008
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ISSN0003-9942
2168-6149
1538-3687
1538-3687
2168-6157
DOI10.1001/archneur.65.5.650

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Summary: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. DESIGN Cross-sectional regression analyses across subjects. SETTING Multicenter, university-based study of subcortical vascular dementia. MAIN OUTCOME MEASURES 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.Arch Neurol. 2008;65(5):650-655-->
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Author Contributions: Study concept and design: Kuczynski, Reed, Mungas, and Jagust. Acquisition of data: Kuczynski, Reed, Mungas, Weiner, Chui, and Jagust. Analysis and interpretation of data: Kuczynski, Reed, Mungas, and Jagust. Drafting of the manuscript: Kuczynski. Critical revision of the manuscript for important intellectual content: Reed, Mungas, Weiner, Chui, and Jagust. Statistical analysis: Kuczynski, Reed, and Mungas. Obtained funding: Kuczynski, Reed, Mungas, and Jagust. Administrative, technical, and material support: Reed, Weiner, Chui, and Jagust. Study supervision: Jagust.
ISSN:0003-9942
2168-6149
1538-3687
1538-3687
2168-6157
DOI:10.1001/archneur.65.5.650