Covariance PET patterns in early Alzheimer's disease and subjects with cognitive impairment but no dementia: utility in group discrimination and correlations with functional performance
Although multivariate analytic techniques might identify diagnostic patterns that are not captured by univariate methods, they have rarely been used to study the neural correlates of Alzheimer's disease (AD) or cognitive impairment. Nonquantitative H 2 15O PET scans were acquired during rest in...
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Published in | NeuroImage (Orlando, Fla.) Vol. 23; no. 1; pp. 35 - 45 |
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Main Authors | , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.09.2004
Elsevier Limited |
Subjects | |
Online Access | Get full text |
ISSN | 1053-8119 1095-9572 1095-9572 |
DOI | 10.1016/j.neuroimage.2004.04.032 |
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Abstract | Although multivariate analytic techniques might identify diagnostic patterns that are not captured by univariate methods, they have rarely been used to study the neural correlates of Alzheimer's disease (AD) or cognitive impairment. Nonquantitative H
2
15O PET scans were acquired during rest in 17 probable AD subjects selected for mild severity [mean-modified Mini Mental Status Examination (mMMS) 46/57; SD 5.1], 16 control subjects (mMMS 54; SD 2.5) and 23 subjects with minimal to mild cognitive impairment but no dementia (mMMS 53; SD 2.8). Expert clinical reading had low success in discriminating AD and controls. There were no significant mean flow differences among groups in traditional univariate SPM Noxel-wise analyses or region of interest (ROI) analyses. A covariance pattern was identified whose mean expression was significantly higher in the AD as compared to controls (
P = 0.03; sensitivity 76–94%; specificity 63–81%). Sites of increased concomitant flow included insula, cuneus, pulvinar, lingual, fusiform, superior occipital and parahippocampal gyri, whereas decreased concomitant flow was found in cingulate, inferior parietal lobule, middle and inferior frontal, supramarginal and precentral gyri. The covariance analysis-derived pattern was then prospectively applied to the cognitively impaired subjects: as compared to subjects with Clinical Dementia Rating (CDR) = 0, subjects with CDR = 0.5 had significantly higher mean covariance pattern expression (
P = 0.009). Expression of this pattern correlated inversely with Selective Reminding Test total recall (
r = −0.401,
P = 0.002), delayed recall (
r = −0.351,
P = 0.008) and mMMS scores (
r = −0.401,
P = 0.002) in all three groups combined. We conclude that patients with AD may differentially express resting cerebral blood flow covariance patterns even at very early disease stages. Significant alterations in expression of resting flow covariance patterns occur even for subjects with cognitive impairment. Expression of covariance patterns correlates with cognitive and functional performance measures, holding promise for meaningful associations with underlying biopathological processes. |
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AbstractList | Although multivariate analytic techniques might identify diagnostic patterns that are not captured by univariate methods, they have rarely been used to study the neural correlates of Alzheimer's disease (AD) or cognitive impairment. Nonquantitative H
2
15O PET scans were acquired during rest in 17 probable AD subjects selected for mild severity [mean-modified Mini Mental Status Examination (mMMS) 46/57; SD 5.1], 16 control subjects (mMMS 54; SD 2.5) and 23 subjects with minimal to mild cognitive impairment but no dementia (mMMS 53; SD 2.8). Expert clinical reading had low success in discriminating AD and controls. There were no significant mean flow differences among groups in traditional univariate SPM Noxel-wise analyses or region of interest (ROI) analyses. A covariance pattern was identified whose mean expression was significantly higher in the AD as compared to controls (
P = 0.03; sensitivity 76–94%; specificity 63–81%). Sites of increased concomitant flow included insula, cuneus, pulvinar, lingual, fusiform, superior occipital and parahippocampal gyri, whereas decreased concomitant flow was found in cingulate, inferior parietal lobule, middle and inferior frontal, supramarginal and precentral gyri. The covariance analysis-derived pattern was then prospectively applied to the cognitively impaired subjects: as compared to subjects with Clinical Dementia Rating (CDR) = 0, subjects with CDR = 0.5 had significantly higher mean covariance pattern expression (
P = 0.009). Expression of this pattern correlated inversely with Selective Reminding Test total recall (
r = −0.401,
P = 0.002), delayed recall (
r = −0.351,
P = 0.008) and mMMS scores (
r = −0.401,
P = 0.002) in all three groups combined. We conclude that patients with AD may differentially express resting cerebral blood flow covariance patterns even at very early disease stages. Significant alterations in expression of resting flow covariance patterns occur even for subjects with cognitive impairment. Expression of covariance patterns correlates with cognitive and functional performance measures, holding promise for meaningful associations with underlying biopathological processes. Although multivariate analytic techniques might identify diagnostic patterns that are not captured by univariate methods, they have rarely been used to study the neural correlates of Alzheimer's disease (AD) or cognitive impairment. Nonquantitative H2(15)O PET scans were acquired during rest in 17 probable AD subjects selected for mild severity [mean-modified Mini Mental Status Examination (mMMS) 46/57; SD 5.1], 16 control subjects (mMMS 54; SD 2.5) and 23 subjects with minimal to mild cognitive impairment but no dementia (mMMS 53; SD 2.8). Expert clinical reading had low success in discriminating AD and controls. There were no significant mean flow differences among groups in traditional univariate SPM Noxel-wise analyses or region of interest (ROI) analyses. A covariance pattern was identified whose mean expression was significantly higher in the AD as compared to controls (P = 0.03; sensitivity 76-94%; specificity 63-81%). Sites of increased concomitant flow included insula, cuneus, pulvinar, lingual, fusiform, superior occipital and parahippocampal gyri, whereas decreased concomitant flow was found in cingulate, inferior parietal lobule, middle and inferior frontal, supramarginal and precentral gyri. The covariance analysis-derived pattern was then prospectively applied to the cognitively impaired subjects: as compared to subjects with Clinical Dementia Rating (CDR) = 0, subjects with CDR = 0.5 had significantly higher mean covariance pattern expression (P = 0.009). Expression of this pattern correlated inversely with Selective Reminding Test total recall (r = -0.401, P = 0.002), delayed recall (r = -0.351, P = 0.008) and mMMS scores (r = -0.401, P = 0.002) in all three groups combined. We conclude that patients with AD may differentially express resting cerebral blood flow covariance patterns even at very early disease stages. Significant alterations in expression of resting flow covariance patterns occur even for subjects with cognitive impairment. Expression of covariance patterns correlates with cognitive and functional performance measures, holding promise for meaningful associations with underlying biopathological processes.Although multivariate analytic techniques might identify diagnostic patterns that are not captured by univariate methods, they have rarely been used to study the neural correlates of Alzheimer's disease (AD) or cognitive impairment. Nonquantitative H2(15)O PET scans were acquired during rest in 17 probable AD subjects selected for mild severity [mean-modified Mini Mental Status Examination (mMMS) 46/57; SD 5.1], 16 control subjects (mMMS 54; SD 2.5) and 23 subjects with minimal to mild cognitive impairment but no dementia (mMMS 53; SD 2.8). Expert clinical reading had low success in discriminating AD and controls. There were no significant mean flow differences among groups in traditional univariate SPM Noxel-wise analyses or region of interest (ROI) analyses. A covariance pattern was identified whose mean expression was significantly higher in the AD as compared to controls (P = 0.03; sensitivity 76-94%; specificity 63-81%). Sites of increased concomitant flow included insula, cuneus, pulvinar, lingual, fusiform, superior occipital and parahippocampal gyri, whereas decreased concomitant flow was found in cingulate, inferior parietal lobule, middle and inferior frontal, supramarginal and precentral gyri. The covariance analysis-derived pattern was then prospectively applied to the cognitively impaired subjects: as compared to subjects with Clinical Dementia Rating (CDR) = 0, subjects with CDR = 0.5 had significantly higher mean covariance pattern expression (P = 0.009). Expression of this pattern correlated inversely with Selective Reminding Test total recall (r = -0.401, P = 0.002), delayed recall (r = -0.351, P = 0.008) and mMMS scores (r = -0.401, P = 0.002) in all three groups combined. We conclude that patients with AD may differentially express resting cerebral blood flow covariance patterns even at very early disease stages. Significant alterations in expression of resting flow covariance patterns occur even for subjects with cognitive impairment. Expression of covariance patterns correlates with cognitive and functional performance measures, holding promise for meaningful associations with underlying biopathological processes. Although multivariate analytic techniques might identify diagnostic patterns that are not captured by univariate methods, they have rarely been used to study the neural correlates of Alzheimer's disease (AD) or cognitive impairment. Nonquantitative H2(15)O PET scans were acquired during rest in 17 probable AD subjects selected for mild severity [mean-modified Mini Mental Status Examination (mMMS) 46/57; SD 5.1], 16 control subjects (mMMS 54; SD 2.5) and 23 subjects with minimal to mild cognitive impairment but no dementia (mMMS 53; SD 2.8). Expert clinical reading had low success in discriminating AD and controls. There were no significant mean flow differences among groups in traditional univariate SPM Noxel-wise analyses or region of interest (ROI) analyses. A covariance pattern was identified whose mean expression was significantly higher in the AD as compared to controls (P = 0.03; sensitivity 76-94%; specificity 63-81%). Sites of increased concomitant flow included insula, cuneus, pulvinar, lingual, fusiform, superior occipital and parahippocampal gyri, whereas decreased concomitant flow was found in cingulate, inferior parietal lobule, middle and inferior frontal, supramarginal and precentral gyri. The covariance analysis-derived pattern was then prospectively applied to the cognitively impaired subjects: as compared to subjects with Clinical Dementia Rating (CDR) = 0, subjects with CDR = 0.5 had significantly higher mean covariance pattern expression (P = 0.009). Expression of this pattern correlated inversely with Selective Reminding Test total recall (r = -0.401, P = 0.002), delayed recall (r = -0.351, P = 0.008) and mMMS scores (r = -0.401, P = 0.002) in all three groups combined. We conclude that patients with AD may differentially express resting cerebral blood flow covariance patterns even at very early disease stages. Significant alterations in expression of resting flow covariance patterns occur even for subjects with cognitive impairment. Expression of covariance patterns correlates with cognitive and functional performance measures, holding promise for meaningful associations with underlying biopathological processes. Although multivariate analytic techniques might identify diagnostic patterns that are not captured by univariate methods, they have rarely been used to study the neural correlates of Alzheimer's disease (AD) or cognitive impairment. Nonquantitative H215O PET scans were acquired during rest in 17 probable AD subjects selected for mild severity [mean-modified Mini Mental Status Examination (mMMS) 46/57; SD 5.1], 16 control subjects (mMMS 54; SD 2.5) and 23 subjects with minimal to mild cognitive impairment but no dementia (mMMS 53; SD 2.8). Expert clinical reading had low success in discriminating AD and controls. There were no significant mean flow differences among groups in traditional univariate SPM Voxel-wise analyses or region of interest (ROI) analyses. A covariance pattern was identified whose mean expression was significantly higher in the AD as compared to controls (P = 0.03; sensitivity 76–94%; specificity 63–81%). Sites of increased concomitant flow included insula, cuneus, pulvinar, lingual, fusiform, superior occipital and parahippocampal gyri, whereas decreased concomitant flow was found in cingulate, inferior parietal lobule, middle and inferior frontal, supramarginal and precentral gyri. The covariance analysis-derived pattern was then prospectively applied to the cognitively impaired subjects: as compared to subjects with Clinical Dementia Rating (CDR) = 0, subjects with CDR = 0.5 had significantly higher mean covariance pattern expression (P = 0.009). Expression of this pattern correlated inversely with Selective Reminding Test total recall (r = −0.401, P = 0.002), delayed recall (r = −0.351, P = 0.008) and mMMS scores (r = −0.401, P = 0.002) in all three groups combined. We conclude that patients with AD may differentially express resting cerebral blood flow covariance patterns even at very early disease stages. Significant alterations in expression of resting flow covariance patterns occur even for subjects with cognitive impairment. Expression of covariance patterns correlates with cognitive and functional performance measures, holding promise for meaningful associations with underlying biopathological processes. Although multivariate analytic techniques might identify diagnostic patterns that are not captured by univariate methods, they have rarely been used to study the neural correlates of Alzheimer's disease (AD) or cognitive impairment. Nonquantitative H215O PET scans were acquired during rest in 17 probable AD subjects selected for mild severity [mean-modified Mini Mental Status Examination (mMMS) 46/57; SD 5.1], 16 control subjects (mMMS 54; SD 2.5) and 23 subjects with minimal to mild cognitive impairment but no dementia (mMMS 53; SD 2.8). Expert clinical reading had low success in discriminating AD and controls. There were no significant mean flow differences among groups in traditional univariate SPM Noxel-wise analyses or region of interest (ROI) analyses. A covariance pattern was identified whose mean expression was significantly higher in the AD as compared to controls (P= 0.03; sensitivity 76-94%; specificity 63-81%). Sites of increased concomitant flow included insula, cuneus, pulvinar, lingual, fusiform, superior occipital and parahippocampal gyri, whereas decreased concomitant flow was found in cingulate, inferior parietal lobule, middle and inferior frontal, supramarginal and precentral gyri. The covariance analysis-derived pattern was then prospectively applied to the cognitively impaired subjects: as compared to subjects with Clinical Dementia Rating (CDR) = 0, subjects with CDR = 0.5 had significantly higher mean covariance pattern expression (P= 0.009). Expression of this pattern correlated inversely with Selective Reminding Test total recall (r= -0.401,P= 0.002), delayed recall (r= -0.351,P= 0.008) and mMMS scores (r= -0.401,P= 0.002) in all three groups combined. We conclude that patients with AD may differentially express resting cerebral blood flow covariance patterns even at very early disease stages. Significant alterations in expression of resting flow covariance patterns occur even for subjects with cognitive impairment. Expression of covariance patterns correlates with cognitive and functional performance measures, holding promise for meaningful associations with underlying biopathological processes. |
Author | Tabert, Matthias H. Park, Aileen Pelton, Gregory H. Stern, Yaakov Devanand, Davangere P. Scarmeas, Nikolaos Zarahn, Eric Hilton, John Anderson, Karen E. Honig, Lawrence S. Habeck, Christian G. Moeller, James R. |
AuthorAffiliation | b Department of Neurology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA a Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA c Department of Psychiatry, University of Maryland, Baltimore, MD 21201, USA d Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA |
AuthorAffiliation_xml | – name: a Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – name: d Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – name: b Department of Neurology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – name: c Department of Psychiatry, University of Maryland, Baltimore, MD 21201, USA |
Author_xml | – sequence: 1 givenname: Nikolaos surname: Scarmeas fullname: Scarmeas, Nikolaos email: ns257@columbia.edu organization: Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 2 givenname: Christian G. surname: Habeck fullname: Habeck, Christian G. organization: Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 3 givenname: Eric surname: Zarahn fullname: Zarahn, Eric organization: Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 4 givenname: Karen E. surname: Anderson fullname: Anderson, Karen E. organization: Department of Psychiatry, University of Maryland, Baltimore, MD 21201, USA – sequence: 5 givenname: Aileen surname: Park fullname: Park, Aileen organization: Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 6 givenname: John surname: Hilton fullname: Hilton, John organization: Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 7 givenname: Gregory H. surname: Pelton fullname: Pelton, Gregory H. organization: Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 8 givenname: Matthias H. surname: Tabert fullname: Tabert, Matthias H. organization: Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 9 givenname: Lawrence S. surname: Honig fullname: Honig, Lawrence S. organization: Department of Neurology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 10 givenname: James R. surname: Moeller fullname: Moeller, James R. organization: Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 11 givenname: Davangere P. surname: Devanand fullname: Devanand, Davangere P. organization: Department of Psychiatry, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA – sequence: 12 givenname: Yaakov surname: Stern fullname: Stern, Yaakov organization: Cognitive Neuroscience Division of the Taub Institute for Research on Alzheimer's Disease and the Aging Brain, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/15325350$$D View this record in MEDLINE/PubMed |
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ContentType | Journal Article |
Copyright | 2004 Elsevier Inc. Copyright Elsevier Limited Sep 1, 2004 |
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SubjectTerms | Aged Alzheimer Disease - diagnostic imaging Alzheimer's disease Analysis of Variance Brain Brain - diagnostic imaging Brain Mapping CBF, diagnosis Cognition Disorders - diagnostic imaging Cognitive Covariance Dementia Diagnosis, Differential Discrimination Dominance, Cerebral - physiology Early Diagnosis Female Humans Image Processing, Computer-Assisted Imaging, Three-Dimensional Male MCI Mental Status Schedule Metabolism Middle Aged Neuropathology PET Positron-Emission Tomography - statistics & numerical data Prospective Studies Reference Values Statistical methods Studies |
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