Principal-Component Analysis-Based Measures of PET Data Closely Reflect Neuropathologic Staging Schemes

Voxel-based principal-component analysis allows for an identification of patterns of glucose metabolism and amyloid deposition related to the conversion from mild cognitive impairment (MCI) to Alzheimer disease (AD). The present study aimed to validate these AD conversion-related patterns (ADCRPs) a...

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Veröffentlicht in:The Journal of nuclear medicine (1978) Jg. 62; H. 6; S. 855
Hauptverfasser: Blazhenets, Ganna, Frings, Lars, Sörensen, Arnd, Meyer, Philipp T
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.06.2021
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Abstract Voxel-based principal-component analysis allows for an identification of patterns of glucose metabolism and amyloid deposition related to the conversion from mild cognitive impairment (MCI) to Alzheimer disease (AD). The present study aimed to validate these AD conversion-related patterns (ADCRPs) against neuropathologic findings. We included patients from the Alzheimer's Disease Neuroimaging Initiative who underwent autopsy and for whom F-FDG PET (30 AD, 6 MCI, 2 cognitively normal) and amyloid-β (Aβ) PET (17 AD, 3 MCI, 2 cognitively normal) were available. Pattern expression scores (PESs) of the F-FDG- and Aβ-ADCRP were compared with Braak tangle stage and Thal amyloid phase, respectively. Mean F-FDG uptake and mean F-AV-45 SUV ratio (SUVr) in regions of hypometabolism and elevated amyloid load typical of AD, respectively, were used as volume-of-interest-based PET measures. The diagnostic performance for identifying none-to-low vs. intermediate-to-high AD neuropathologic change (ADNC) was assessed for all biomarkers. We observed significant associations between PES of F-FDG-ADCRP and Braak stage (ρ > 0.48, < 0.005) and between PES of Aβ-ADCRP and Thal phase (ρ > 0.66, < 0.001). PES of F-FDG-ADCRP, PES of Aβ-ADCRP, and their combination identified intermediate-to-high ADNC with an area under the receiver-operating-characteristic curve (AUC) of 0.80, 0.95, and 0.98 ( = 22), respectively. Mean F-FDG uptake and mean F-AV-45 SUVr in AD-typical regions were also significantly associated with Braak stage (|ρ| > 0.45, < 0.01) and Thal phase (ρ > 0.55, < 0.01), respectively. Volume-of-interest-based PET measures discriminated between ADNC stages with an AUC of 0.79, 0.88, and 0.90 for mean F-FDG uptake, mean F-AV-45 SUVr, and their combination ( = 22), respectively. Contemplating all subjects with available F-FDG PET and neuropathology information ( = 38), PES of F-FDG-ADCRP was a significant predictor of intermediate-to-high ADNC (AUC = 0.72), whereas mean F-FDG uptake was not (AUC = 0.66), although the difference between methods was not significant. PES of F-FDG-ADCRP, a measure of neurodegeneration, shows close correspondence with the extent of tau pathology, as assessed by Braak tangle stage. PES of Aβ-ADCRP is a valid biomarker of underlying amyloid pathology, as demonstrated by its strong correlation with Thal phase. The combination of ADCRPs performed better than F-FDG-ADCRP alone, although there was only negligible improvement compared with Aβ-ADCRP.
AbstractList Voxel-based principal-component analysis allows for an identification of patterns of glucose metabolism and amyloid deposition related to the conversion from mild cognitive impairment (MCI) to Alzheimer disease (AD). The present study aimed to validate these AD conversion-related patterns (ADCRPs) against neuropathologic findings. We included patients from the Alzheimer's Disease Neuroimaging Initiative who underwent autopsy and for whom F-FDG PET (30 AD, 6 MCI, 2 cognitively normal) and amyloid-β (Aβ) PET (17 AD, 3 MCI, 2 cognitively normal) were available. Pattern expression scores (PESs) of the F-FDG- and Aβ-ADCRP were compared with Braak tangle stage and Thal amyloid phase, respectively. Mean F-FDG uptake and mean F-AV-45 SUV ratio (SUVr) in regions of hypometabolism and elevated amyloid load typical of AD, respectively, were used as volume-of-interest-based PET measures. The diagnostic performance for identifying none-to-low vs. intermediate-to-high AD neuropathologic change (ADNC) was assessed for all biomarkers. We observed significant associations between PES of F-FDG-ADCRP and Braak stage (ρ > 0.48, < 0.005) and between PES of Aβ-ADCRP and Thal phase (ρ > 0.66, < 0.001). PES of F-FDG-ADCRP, PES of Aβ-ADCRP, and their combination identified intermediate-to-high ADNC with an area under the receiver-operating-characteristic curve (AUC) of 0.80, 0.95, and 0.98 ( = 22), respectively. Mean F-FDG uptake and mean F-AV-45 SUVr in AD-typical regions were also significantly associated with Braak stage (|ρ| > 0.45, < 0.01) and Thal phase (ρ > 0.55, < 0.01), respectively. Volume-of-interest-based PET measures discriminated between ADNC stages with an AUC of 0.79, 0.88, and 0.90 for mean F-FDG uptake, mean F-AV-45 SUVr, and their combination ( = 22), respectively. Contemplating all subjects with available F-FDG PET and neuropathology information ( = 38), PES of F-FDG-ADCRP was a significant predictor of intermediate-to-high ADNC (AUC = 0.72), whereas mean F-FDG uptake was not (AUC = 0.66), although the difference between methods was not significant. PES of F-FDG-ADCRP, a measure of neurodegeneration, shows close correspondence with the extent of tau pathology, as assessed by Braak tangle stage. PES of Aβ-ADCRP is a valid biomarker of underlying amyloid pathology, as demonstrated by its strong correlation with Thal phase. The combination of ADCRPs performed better than F-FDG-ADCRP alone, although there was only negligible improvement compared with Aβ-ADCRP.
Voxel-based principal-component analysis allows for an identification of patterns of glucose metabolism and amyloid deposition related to the conversion from mild cognitive impairment (MCI) to Alzheimer disease (AD). The present study aimed to validate these AD conversion-related patterns (ADCRPs) against neuropathologic findings. Methods: We included patients from the Alzheimer's Disease Neuroimaging Initiative who underwent autopsy and for whom 18F-FDG PET (30 AD, 6 MCI, 2 cognitively normal) and amyloid-β (Aβ) PET (17 AD, 3 MCI, 2 cognitively normal) were available. Pattern expression scores (PESs) of the 18F-FDG- and Aβ-ADCRP were compared with Braak tangle stage and Thal amyloid phase, respectively. Mean 18F-FDG uptake and mean 18F-AV-45 SUV ratio (SUVr) in regions of hypometabolism and elevated amyloid load typical of AD, respectively, were used as volume-of-interest-based PET measures. The diagnostic performance for identifying none-to-low vs. intermediate-to-high AD neuropathologic change (ADNC) was assessed for all biomarkers. Results: We observed significant associations between PES of 18F-FDG-ADCRP and Braak stage (ρ > 0.48, P < 0.005) and between PES of Aβ-ADCRP and Thal phase (ρ > 0.66, P < 0.001). PES of 18F-FDG-ADCRP, PES of Aβ-ADCRP, and their combination identified intermediate-to-high ADNC with an area under the receiver-operating-characteristic curve (AUC) of 0.80, 0.95, and 0.98 (n = 22), respectively. Mean 18F-FDG uptake and mean 18F-AV-45 SUVr in AD-typical regions were also significantly associated with Braak stage (|ρ| > 0.45, P < 0.01) and Thal phase (ρ > 0.55, P < 0.01), respectively. Volume-of-interest-based PET measures discriminated between ADNC stages with an AUC of 0.79, 0.88, and 0.90 for mean 18F-FDG uptake, mean 18F-AV-45 SUVr, and their combination (n = 22), respectively. Contemplating all subjects with available 18F-FDG PET and neuropathology information (n = 38), PES of 18F-FDG-ADCRP was a significant predictor of intermediate-to-high ADNC (AUC = 0.72), whereas mean 18F-FDG uptake was not (AUC = 0.66), although the difference between methods was not significant. Conclusion: PES of 18F-FDG-ADCRP, a measure of neurodegeneration, shows close correspondence with the extent of tau pathology, as assessed by Braak tangle stage. PES of Aβ-ADCRP is a valid biomarker of underlying amyloid pathology, as demonstrated by its strong correlation with Thal phase. The combination of ADCRPs performed better than 18F-FDG-ADCRP alone, although there was only negligible improvement compared with Aβ-ADCRP.Voxel-based principal-component analysis allows for an identification of patterns of glucose metabolism and amyloid deposition related to the conversion from mild cognitive impairment (MCI) to Alzheimer disease (AD). The present study aimed to validate these AD conversion-related patterns (ADCRPs) against neuropathologic findings. Methods: We included patients from the Alzheimer's Disease Neuroimaging Initiative who underwent autopsy and for whom 18F-FDG PET (30 AD, 6 MCI, 2 cognitively normal) and amyloid-β (Aβ) PET (17 AD, 3 MCI, 2 cognitively normal) were available. Pattern expression scores (PESs) of the 18F-FDG- and Aβ-ADCRP were compared with Braak tangle stage and Thal amyloid phase, respectively. Mean 18F-FDG uptake and mean 18F-AV-45 SUV ratio (SUVr) in regions of hypometabolism and elevated amyloid load typical of AD, respectively, were used as volume-of-interest-based PET measures. The diagnostic performance for identifying none-to-low vs. intermediate-to-high AD neuropathologic change (ADNC) was assessed for all biomarkers. Results: We observed significant associations between PES of 18F-FDG-ADCRP and Braak stage (ρ > 0.48, P < 0.005) and between PES of Aβ-ADCRP and Thal phase (ρ > 0.66, P < 0.001). PES of 18F-FDG-ADCRP, PES of Aβ-ADCRP, and their combination identified intermediate-to-high ADNC with an area under the receiver-operating-characteristic curve (AUC) of 0.80, 0.95, and 0.98 (n = 22), respectively. Mean 18F-FDG uptake and mean 18F-AV-45 SUVr in AD-typical regions were also significantly associated with Braak stage (|ρ| > 0.45, P < 0.01) and Thal phase (ρ > 0.55, P < 0.01), respectively. Volume-of-interest-based PET measures discriminated between ADNC stages with an AUC of 0.79, 0.88, and 0.90 for mean 18F-FDG uptake, mean 18F-AV-45 SUVr, and their combination (n = 22), respectively. Contemplating all subjects with available 18F-FDG PET and neuropathology information (n = 38), PES of 18F-FDG-ADCRP was a significant predictor of intermediate-to-high ADNC (AUC = 0.72), whereas mean 18F-FDG uptake was not (AUC = 0.66), although the difference between methods was not significant. Conclusion: PES of 18F-FDG-ADCRP, a measure of neurodegeneration, shows close correspondence with the extent of tau pathology, as assessed by Braak tangle stage. PES of Aβ-ADCRP is a valid biomarker of underlying amyloid pathology, as demonstrated by its strong correlation with Thal phase. The combination of ADCRPs performed better than 18F-FDG-ADCRP alone, although there was only negligible improvement compared with Aβ-ADCRP.
Author Sörensen, Arnd
Meyer, Philipp T
Blazhenets, Ganna
Frings, Lars
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conversion pattern
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Braak tangle stage
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Snippet Voxel-based principal-component analysis allows for an identification of patterns of glucose metabolism and amyloid deposition related to the conversion from...
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SubjectTerms Aged
Alzheimer Disease - diagnostic imaging
Alzheimer Disease - metabolism
Alzheimer Disease - pathology
Cognitive Dysfunction - diagnostic imaging
Cognitive Dysfunction - metabolism
Cognitive Dysfunction - pathology
Female
Fluorodeoxyglucose F18
Humans
Image Processing, Computer-Assisted - methods
Male
Middle Aged
Neuroimaging
Positron-Emission Tomography
Principal Component Analysis
Title Principal-Component Analysis-Based Measures of PET Data Closely Reflect Neuropathologic Staging Schemes
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