Cognitive and anatomic contributions of metabolic decline in Alzheimer disease and cerebrovascular disease

Beth Kuczynski, Bruce R Reed, Dan M Mungas, Michael Weiner, Helena C. Chui, William Jagust

Research output: Contribution to journalArticle

34 Citations (Scopus)

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. 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.

Original languageEnglish (US)
Pages (from-to)650-655
Number of pages6
JournalArchives of Neurology
Volume65
Issue number5
DOIs
StatePublished - May 2008

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Cerebrovascular Disorders
Positron-Emission Tomography
Executive Function
Alzheimer Disease
Dementia
Episodic Memory
Cognition
Glucose
Vascular Dementia
Brain
Frontal Lobe
Anatomy
Cross-Sectional Studies
Regression Analysis
Outcome Assessment (Health Care)
White Matter
Alzheimer's Disease
Positron Emission Tomography
Metabolism
Cognitive Dysfunction

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Cognitive and anatomic contributions of metabolic decline in Alzheimer disease and cerebrovascular disease. / Kuczynski, Beth; Reed, Bruce R; Mungas, Dan M; Weiner, Michael; Chui, Helena C.; Jagust, William.

In: Archives of Neurology, Vol. 65, No. 5, 05.2008, p. 650-655.

Research output: Contribution to journalArticle

Kuczynski, Beth ; Reed, Bruce R ; Mungas, Dan M ; Weiner, Michael ; Chui, Helena C. ; Jagust, William. / Cognitive and anatomic contributions of metabolic decline in Alzheimer disease and cerebrovascular disease. In: Archives of Neurology. 2008 ; Vol. 65, No. 5. pp. 650-655.
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