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
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.
Kuczynski
Beth
B
Helen Wills Neuroscience Institute and the Lawrence Berkeley National Laboratory, University of California, Berkeley, CA 94720, USA. beth.kuczynski@gmail.com
Reed
Bruce
B
Mungas
Dan
D
Weiner
Michael
M
Chui
Helena C
HC
Jagust
William
W
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
D005947:Glucose