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 in | Archives of neurology (Chicago) Vol. 65; no. 5; pp. 650 - 655 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Chicago, IL
American Medical Association
01.05.2008
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Subjects | |
Online Access | Get full text |
ISSN | 0003-9942 2168-6149 1538-3687 1538-3687 2168-6157 |
DOI | 10.1001/archneur.65.5.650 |
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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.Arch Neurol. 2008;65(5):650-655--> |
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AbstractList | 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.BACKGROUNDAlzheimer 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.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.OBJECTIVETo 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.Cross-sectional regression analyses across subjects.DESIGNCross-sectional regression analyses across subjects.Multicenter, university-based study of subcortical vascular dementia.SETTINGMulticenter, university-based study of subcortical vascular dementia.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.MAIN OUTCOME MEASURESRegional 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.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).RESULTSLow 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).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.CONCLUSIONSLow 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. 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--> 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. 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. Cross-sectional regression analyses across subjects. Multicenter, university-based study of subcortical vascular dementia. 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. 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). 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. 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. 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. Cross-sectional regression analyses across subjects. Multicenter, university-based study of subcortical vascular dementia. 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. 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). 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. |
Author | Chui, Helena C Mungas, Dan Jagust, William Kuczynski, Beth Reed, Bruce Weiner, Michael |
AuthorAffiliation | Helen Wills Neuroscience Institute and the Lawrence Berkeley National Laboratory, University of California, Berkeley (Drs Kuczynski and Jagust); Alzheimer's Disease Center, University of California, Davis, and Northern California Veterans Affairs Health Care System, Sacramento (Drs Reed and Mungas); Department of Veterans Affairs Medical Center, University of California, San Francisco (Dr Weiner); and Department of Neurology, University of Southern California, Los Angeles (Dr Chui) |
AuthorAffiliation_xml | – name: Helen Wills Neuroscience Institute and the Lawrence Berkeley National Laboratory, University of California, Berkeley (Drs Kuczynski and Jagust); Alzheimer's Disease Center, University of California, Davis, and Northern California Veterans Affairs Health Care System, Sacramento (Drs Reed and Mungas); Department of Veterans Affairs Medical Center, University of California, San Francisco (Dr Weiner); and Department of Neurology, University of Southern California, Los Angeles (Dr Chui) |
Author_xml | – sequence: 1 givenname: Beth surname: Kuczynski fullname: Kuczynski, Beth – sequence: 2 givenname: Bruce surname: Reed fullname: Reed, Bruce – sequence: 3 givenname: Dan surname: Mungas fullname: Mungas, Dan – sequence: 4 givenname: Michael surname: Weiner fullname: Weiner, Michael – sequence: 5 givenname: Helena C surname: Chui fullname: Chui, Helena C – sequence: 6 givenname: William surname: Jagust fullname: Jagust, William |
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Keywords | Nervous system diseases Alzheimer disease Central nervous system disease Metabolic diseases Degenerative disease Cerebrovascular disease Cerebral disorder |
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Notes | SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 14 ObjectType-Article-1 ObjectType-Feature-2 content type line 23 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. |
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Snippet | BACKGROUND Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive... Alzheimer disease and cerebrovascular disease affect elderly persons through alterations in brain structure and metabolism that produce cognitive decline.... |
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SubjectTerms | Aged Aged, 80 and over Alzheimer Disease - diagnostic imaging Alzheimer Disease - metabolism Alzheimer Disease - pathology Alzheimer's disease Atrophy - diagnostic imaging Atrophy - metabolism Atrophy - pathology Biological and medical sciences Brain Brain - diagnostic imaging Brain - metabolism Brain - pathology Brain Diseases, Metabolic - diagnostic imaging Brain Diseases, Metabolic - metabolism Brain Diseases, Metabolic - pathology Brain Mapping Cognition & reasoning Cognition Disorders - diagnostic imaging Cognition Disorders - metabolism Cognition Disorders - pathology Cross-Sectional Studies Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases Dementia, Vascular - diagnostic imaging Dementia, Vascular - metabolism Dementia, Vascular - pathology Disease Progression Energy Metabolism - physiology Female Geriatrics Glucose - metabolism Hippocampus - diagnostic imaging Hippocampus - metabolism Hippocampus - pathology Humans Male Medical sciences Memory Disorders - diagnostic imaging Memory Disorders - metabolism Memory Disorders - pathology Nerve Fibers, Myelinated - metabolism Nerve Fibers, Myelinated - pathology Neurology Neuropsychological Tests Older people Original Contribution Positron-Emission Tomography Predictive Value of Tests Regression analysis Studies |
Title | Cognitive and Anatomic Contributions of Metabolic Decline in Alzheimer Disease and Cerebrovascular Disease |
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