Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative

Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with n...
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Autor*in:	Canevelli, Marco [verfasserIn] Arisi, Ivan [verfasserIn] Bacigalupo, Ilaria [verfasserIn] Arighi, Andrea [verfasserIn] Galimberti, Daniela [verfasserIn] Vanacore, Nicola [verfasserIn] D’Onofrio, Mara [verfasserIn] Cesari, Matteo [verfasserIn] Bruno, Giuseppe [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Alzheimer’s disease Frailty Biomarkers Aging Dementia

Übergeordnetes Werk:	Enthalten in: Age - New York, NY : Springer Science+Business Media, 1978, 43(2020), 2 vom: 19. Nov., Seite 1039-1051
Übergeordnetes Werk:	volume:43 ; year:2020 ; number:2 ; day:19 ; month:11 ; pages:1039-1051

Links:	Volltext

DOI / URN:	10.1007/s11357-020-00293-y

Katalog-ID:	SPR04399721X

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allfields	10.1007/s11357-020-00293-y doi (DE-627)SPR04399721X (DE-599)SPRs11357-020-00293-y-e (SPR)s11357-020-00293-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.68 bkl Canevelli, Marco verfasserin aut Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF $ Aβ_{1-42} $, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of $ Aβ_{1-42} $, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes. Alzheimer’s disease (dpeaa)DE-He213 Frailty (dpeaa)DE-He213 Biomarkers (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Dementia (dpeaa)DE-He213 Arisi, Ivan verfasserin aut Bacigalupo, Ilaria verfasserin aut Arighi, Andrea verfasserin aut Galimberti, Daniela verfasserin aut Vanacore, Nicola verfasserin aut D’Onofrio, Mara verfasserin aut Cesari, Matteo verfasserin aut Bruno, Giuseppe verfasserin aut Enthalten in Age New York, NY : Springer Science+Business Media, 1978 43(2020), 2 vom: 19. Nov., Seite 1039-1051 (DE-627)499546180 (DE-600)2201958-3 1574-4647 nnns volume:43 year:2020 number:2 day:19 month:11 pages:1039-1051 https://dx.doi.org/10.1007/s11357-020-00293-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_40 GBV_ILN_60 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_110 GBV_ILN_120 GBV_ILN_161 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 44.68 ASE AR 43 2020 2 19 11 1039-1051
spelling	10.1007/s11357-020-00293-y doi (DE-627)SPR04399721X (DE-599)SPRs11357-020-00293-y-e (SPR)s11357-020-00293-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.68 bkl Canevelli, Marco verfasserin aut Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF $ Aβ_{1-42} $, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of $ Aβ_{1-42} $, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes. Alzheimer’s disease (dpeaa)DE-He213 Frailty (dpeaa)DE-He213 Biomarkers (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Dementia (dpeaa)DE-He213 Arisi, Ivan verfasserin aut Bacigalupo, Ilaria verfasserin aut Arighi, Andrea verfasserin aut Galimberti, Daniela verfasserin aut Vanacore, Nicola verfasserin aut D’Onofrio, Mara verfasserin aut Cesari, Matteo verfasserin aut Bruno, Giuseppe verfasserin aut Enthalten in Age New York, NY : Springer Science+Business Media, 1978 43(2020), 2 vom: 19. Nov., Seite 1039-1051 (DE-627)499546180 (DE-600)2201958-3 1574-4647 nnns volume:43 year:2020 number:2 day:19 month:11 pages:1039-1051 https://dx.doi.org/10.1007/s11357-020-00293-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_40 GBV_ILN_60 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_110 GBV_ILN_120 GBV_ILN_161 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 44.68 ASE AR 43 2020 2 19 11 1039-1051
allfields_unstemmed	10.1007/s11357-020-00293-y doi (DE-627)SPR04399721X (DE-599)SPRs11357-020-00293-y-e (SPR)s11357-020-00293-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.68 bkl Canevelli, Marco verfasserin aut Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF $ Aβ_{1-42} $, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of $ Aβ_{1-42} $, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes. Alzheimer’s disease (dpeaa)DE-He213 Frailty (dpeaa)DE-He213 Biomarkers (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Dementia (dpeaa)DE-He213 Arisi, Ivan verfasserin aut Bacigalupo, Ilaria verfasserin aut Arighi, Andrea verfasserin aut Galimberti, Daniela verfasserin aut Vanacore, Nicola verfasserin aut D’Onofrio, Mara verfasserin aut Cesari, Matteo verfasserin aut Bruno, Giuseppe verfasserin aut Enthalten in Age New York, NY : Springer Science+Business Media, 1978 43(2020), 2 vom: 19. Nov., Seite 1039-1051 (DE-627)499546180 (DE-600)2201958-3 1574-4647 nnns volume:43 year:2020 number:2 day:19 month:11 pages:1039-1051 https://dx.doi.org/10.1007/s11357-020-00293-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_40 GBV_ILN_60 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_110 GBV_ILN_120 GBV_ILN_161 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 44.68 ASE AR 43 2020 2 19 11 1039-1051
allfieldsGer	10.1007/s11357-020-00293-y doi (DE-627)SPR04399721X (DE-599)SPRs11357-020-00293-y-e (SPR)s11357-020-00293-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.68 bkl Canevelli, Marco verfasserin aut Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF $ Aβ_{1-42} $, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of $ Aβ_{1-42} $, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes. Alzheimer’s disease (dpeaa)DE-He213 Frailty (dpeaa)DE-He213 Biomarkers (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Dementia (dpeaa)DE-He213 Arisi, Ivan verfasserin aut Bacigalupo, Ilaria verfasserin aut Arighi, Andrea verfasserin aut Galimberti, Daniela verfasserin aut Vanacore, Nicola verfasserin aut D’Onofrio, Mara verfasserin aut Cesari, Matteo verfasserin aut Bruno, Giuseppe verfasserin aut Enthalten in Age New York, NY : Springer Science+Business Media, 1978 43(2020), 2 vom: 19. Nov., Seite 1039-1051 (DE-627)499546180 (DE-600)2201958-3 1574-4647 nnns volume:43 year:2020 number:2 day:19 month:11 pages:1039-1051 https://dx.doi.org/10.1007/s11357-020-00293-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_40 GBV_ILN_60 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_110 GBV_ILN_120 GBV_ILN_161 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 44.68 ASE AR 43 2020 2 19 11 1039-1051
allfieldsSound	10.1007/s11357-020-00293-y doi (DE-627)SPR04399721X (DE-599)SPRs11357-020-00293-y-e (SPR)s11357-020-00293-y-e DE-627 ger DE-627 rakwb eng 610 ASE 44.68 bkl Canevelli, Marco verfasserin aut Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF $ Aβ_{1-42} $, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of $ Aβ_{1-42} $, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes. Alzheimer’s disease (dpeaa)DE-He213 Frailty (dpeaa)DE-He213 Biomarkers (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Dementia (dpeaa)DE-He213 Arisi, Ivan verfasserin aut Bacigalupo, Ilaria verfasserin aut Arighi, Andrea verfasserin aut Galimberti, Daniela verfasserin aut Vanacore, Nicola verfasserin aut D’Onofrio, Mara verfasserin aut Cesari, Matteo verfasserin aut Bruno, Giuseppe verfasserin aut Enthalten in Age New York, NY : Springer Science+Business Media, 1978 43(2020), 2 vom: 19. Nov., Seite 1039-1051 (DE-627)499546180 (DE-600)2201958-3 1574-4647 nnns volume:43 year:2020 number:2 day:19 month:11 pages:1039-1051 https://dx.doi.org/10.1007/s11357-020-00293-y kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_40 GBV_ILN_60 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_110 GBV_ILN_120 GBV_ILN_161 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_647 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2106 GBV_ILN_2108 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_2232 44.68 ASE AR 43 2020 2 19 11 1039-1051
language	English
source	Enthalten in Age 43(2020), 2 vom: 19. Nov., Seite 1039-1051 volume:43 year:2020 number:2 day:19 month:11 pages:1039-1051
sourceStr	Enthalten in Age 43(2020), 2 vom: 19. Nov., Seite 1039-1051 volume:43 year:2020 number:2 day:19 month:11 pages:1039-1051
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Alzheimer’s disease Frailty Biomarkers Aging Dementia
dewey-raw	610
isfreeaccess_bool	true
container_title	Age
authorswithroles_txt_mv	Canevelli, Marco @@aut@@ Arisi, Ivan @@aut@@ Bacigalupo, Ilaria @@aut@@ Arighi, Andrea @@aut@@ Galimberti, Daniela @@aut@@ Vanacore, Nicola @@aut@@ D’Onofrio, Mara @@aut@@ Cesari, Matteo @@aut@@ Bruno, Giuseppe @@aut@@
publishDateDaySort_date	2020-11-19T00:00:00Z
hierarchy_top_id	499546180
dewey-sort	3610
id	SPR04399721X
language_de	englisch
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author	Canevelli, Marco
spellingShingle	Canevelli, Marco ddc 610 bkl 44.68 misc Alzheimer’s disease misc Frailty misc Biomarkers misc Aging misc Dementia Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative
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topic_title	610 ASE 44.68 bkl Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative Alzheimer’s disease (dpeaa)DE-He213 Frailty (dpeaa)DE-He213 Biomarkers (dpeaa)DE-He213 Aging (dpeaa)DE-He213 Dementia (dpeaa)DE-He213
topic	ddc 610 bkl 44.68 misc Alzheimer’s disease misc Frailty misc Biomarkers misc Aging misc Dementia
topic_unstemmed	ddc 610 bkl 44.68 misc Alzheimer’s disease misc Frailty misc Biomarkers misc Aging misc Dementia
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title	Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative
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title_full	Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative
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author_browse	Canevelli, Marco Arisi, Ivan Bacigalupo, Ilaria Arighi, Andrea Galimberti, Daniela Vanacore, Nicola D’Onofrio, Mara Cesari, Matteo Bruno, Giuseppe
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title_sort	biomarkers and phenotypic expression in alzheimer’s disease: exploring the contribution of frailty in the alzheimer’s disease neuroimaging initiative
title_auth	Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative
abstract	Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF $ Aβ_{1-42} $, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of $ Aβ_{1-42} $, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes.
abstractGer	Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF $ Aβ_{1-42} $, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of $ Aβ_{1-42} $, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes.
abstract_unstemmed	Abstract The present study aimed at investigating if the main biomarkers of Alzheimer’s disease (AD) neuropathology and their association with cognitive disturbances and dementia are modified by the individual’s frailty status. We performed a cross-sectional analysis of data from participants with normal cognition, mild cognitive impairment (MCI), and AD dementia enrolled in the Alzheimer’s Disease Neuroimaging Initiative 2 (ADNI2) study. Frailty was operationalized by computing a 40-item Frailty Index (FI). The following AD biomarkers were considered and analyzed according to the participants’ frailty status: CSF $ Aβ_{1-42} $, 181P-tau, and T-tau; MRI-based hippocampus volume; cortical glucose metabolism at the FDG PET imaging; amyloid deposition at the 18F-AV-45 PET imaging. Logistic regression models, adjusted for age, sex, and education, were performed to explore the association of biomarkers with cognitive status at different FI levels. Subjects with higher FI scores had lower CSF levels of $ Aβ_{1-42} $, hippocampus volumes at the MRI, and glucose metabolism at the FDG PET imaging, and a higher amyloid deposition at the 18F-AV-45 PET. No significant differences were observed among the two frailty groups concerning ApoE genotype, CSF T-tau, and P-tau. Increasing frailty levels were associated with a weakened relationship between dementia and 18F-AV-45 uptake and hippocampus volume and with a stronger relationship of dementia with FDG PET. Frailty contributes to the discrepancies between AD pathology and clinical manifestations and influences the association of AD pathological modifications with cognitive changes. AD and dementia should increasingly be conceived as “complex diseases of aging,” determined by multiple, simultaneous, and interacting pathophysiological processes.
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title_short	Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative
url	https://dx.doi.org/10.1007/s11357-020-00293-y
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author2	Arisi, Ivan Bacigalupo, Ilaria Arighi, Andrea Galimberti, Daniela Vanacore, Nicola D’Onofrio, Mara Cesari, Matteo Bruno, Giuseppe
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Biomarkers and phenotypic expression in Alzheimer’s disease: exploring the contribution of frailty in the Alzheimer’s Disease Neuroimaging Initiative

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