Weight loss in the healthy elderly might be a non-cognitive sign of preclinical Alzheimer's disease
Weight loss has been proposed as a sign of pre-clinical Alzheimer Disease (AD). To test this hypothesis, we have evaluated the association between longitudinal changes in weight trajectories, cognitive performance, AD biomarker profiles and brain structure in 363 healthy controls from the Alzheimer´...
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Published in | Oncotarget Vol. 8; no. 62; pp. 104706 - 104716 |
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Main Authors | , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Impact Journals LLC
01.12.2017
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ISSN | 1949-2553 1949-2553 |
DOI | 10.18632/oncotarget.22218 |
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Abstract | Weight loss has been proposed as a sign of pre-clinical Alzheimer Disease (AD). To test this hypothesis, we have evaluated the association between longitudinal changes in weight trajectories, cognitive performance, AD biomarker profiles and brain structure in 363 healthy controls from the Alzheimer´s Disease Neuroimaging Initiative (mean follow-up 50.5±30.5 months). Subjects were classified according to body weight trajectory into a weight loss group (WLG; relative weight loss ≥ 5%) and a non-weight loss group (non-WLG; relative weight loss < 5%). Linear mixed effects models were used to estimate the effect of body weight changes on ADAS-Cognitive score across time. Baseline CSF tau/AΔ
ratio and AV45 PET uptake were compared between WLG and non-WLG by analysis of covariance. Atrophy maps were compared between groups at baseline and longitudinally at a 2-year follow-up using Freesurfer. WLG showed increased baseline levels of cerebrospinal fluid tau/AΔ
ratio, increased PET amyloid uptake and diminished cortical thickness at baseline. WLG also showed faster cognitive decline and faster longitudinal atrophy. Our data support weight loss as a non-cognitive manifestation of pre-clinical AD. |
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AbstractList | Weight loss has been proposed as a sign of pre-clinical Alzheimer Disease (AD). To test this hypothesis, we have evaluated the association between longitudinal changes in weight trajectories, cognitive performance, AD biomarker profiles and brain structure in 363 healthy controls from the Alzheimer´s Disease Neuroimaging Initiative (mean follow-up 50.5±30.5 months). Subjects were classified according to body weight trajectory into a weight loss group (WLG; relative weight loss ≥ 5%) and a non-weight loss group (non-WLG; relative weight loss < 5%). Linear mixed effects models were used to estimate the effect of body weight changes on ADAS-Cognitive score across time. Baseline CSF tau/AΔ42 ratio and AV45 PET uptake were compared between WLG and non-WLG by analysis of covariance. Atrophy maps were compared between groups at baseline and longitudinally at a 2-year follow-up using Freesurfer. WLG showed increased baseline levels of cerebrospinal fluid tau/AΔ42 ratio, increased PET amyloid uptake and diminished cortical thickness at baseline. WLG also showed faster cognitive decline and faster longitudinal atrophy. Our data support weight loss as a non-cognitive manifestation of pre-clinical AD.Weight loss has been proposed as a sign of pre-clinical Alzheimer Disease (AD). To test this hypothesis, we have evaluated the association between longitudinal changes in weight trajectories, cognitive performance, AD biomarker profiles and brain structure in 363 healthy controls from the Alzheimer´s Disease Neuroimaging Initiative (mean follow-up 50.5±30.5 months). Subjects were classified according to body weight trajectory into a weight loss group (WLG; relative weight loss ≥ 5%) and a non-weight loss group (non-WLG; relative weight loss < 5%). Linear mixed effects models were used to estimate the effect of body weight changes on ADAS-Cognitive score across time. Baseline CSF tau/AΔ42 ratio and AV45 PET uptake were compared between WLG and non-WLG by analysis of covariance. Atrophy maps were compared between groups at baseline and longitudinally at a 2-year follow-up using Freesurfer. WLG showed increased baseline levels of cerebrospinal fluid tau/AΔ42 ratio, increased PET amyloid uptake and diminished cortical thickness at baseline. WLG also showed faster cognitive decline and faster longitudinal atrophy. Our data support weight loss as a non-cognitive manifestation of pre-clinical AD. Weight loss has been proposed as a sign of pre-clinical Alzheimer Disease (AD). To test this hypothesis, we have evaluated the association between longitudinal changes in weight trajectories, cognitive performance, AD biomarker profiles and brain structure in 363 healthy controls from the Alzheimer´s Disease Neuroimaging Initiative (mean follow-up 50.5±30.5 months). Subjects were classified according to body weight trajectory into a weight loss group (WLG; relative weight loss ≥ 5%) and a non-weight loss group (non-WLG; relative weight loss < 5%). Linear mixed effects models were used to estimate the effect of body weight changes on ADAS-Cognitive score across time. Baseline CSF tau/AΔ ratio and AV45 PET uptake were compared between WLG and non-WLG by analysis of covariance. Atrophy maps were compared between groups at baseline and longitudinally at a 2-year follow-up using Freesurfer. WLG showed increased baseline levels of cerebrospinal fluid tau/AΔ ratio, increased PET amyloid uptake and diminished cortical thickness at baseline. WLG also showed faster cognitive decline and faster longitudinal atrophy. Our data support weight loss as a non-cognitive manifestation of pre-clinical AD. Weight loss has been proposed as a sign of pre-clinical Alzheimer Disease (AD). To test this hypothesis, we have evaluated the association between longitudinal changes in weight trajectories, cognitive performance, AD biomarker profiles and brain structure in 363 healthy controls from the Alzheimer´s Disease Neuroimaging Initiative (mean follow-up 50.5±30.5 months). Subjects were classified according to body weight trajectory into a weight loss group (WLG; relative weight loss ≥ 5%) and a non-weight loss group (non-WLG; relative weight loss < 5%). Linear mixed effects models were used to estimate the effect of body weight changes on ADAS-Cognitive score across time. Baseline CSF tau/AΔ 42 ratio and AV45 PET uptake were compared between WLG and non-WLG by analysis of covariance. Atrophy maps were compared between groups at baseline and longitudinally at a 2-year follow-up using Freesurfer. WLG showed increased baseline levels of cerebrospinal fluid tau/AΔ 42 ratio, increased PET amyloid uptake and diminished cortical thickness at baseline. WLG also showed faster cognitive decline and faster longitudinal atrophy. Our data support weight loss as a non-cognitive manifestation of pre-clinical AD. |
Author | Blesa, Rafael Pané, Adriana Jimenez, Amanda Carmona-Iragui, María Vidal, Josep Belbin, Olivia Moizé, Violeta Montal, Victor Alcolea, Daniel Fortea, Juan Pegueroles, Jordi Vilaplana, Eduard Casajoana, Anna Videla, Laura Illán-Gala, Ignacio Clarimón, Jordi Lleó, Alberto |
AuthorAffiliation | 1 Endocrinology and Diabetes Department, Obesity Unit, Hospital Clinic de Barcelona, Barcelona, Spain 4 Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain 3 Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain 2 Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona, Spain 5 Barcelona Down Medical Center, Fundació Catalana de Síndrome de Down, Barcelona, Spain 6 General Surgery Service, Hospital de Barcelona-SCIAS, Barcelona, Spain 7 Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain |
AuthorAffiliation_xml | – name: 1 Endocrinology and Diabetes Department, Obesity Unit, Hospital Clinic de Barcelona, Barcelona, Spain – name: 3 Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain – name: 4 Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – name: 2 Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona, Spain – name: 7 Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain – name: 6 General Surgery Service, Hospital de Barcelona-SCIAS, Barcelona, Spain – name: 5 Barcelona Down Medical Center, Fundació Catalana de Síndrome de Down, Barcelona, Spain |
Author_xml | – sequence: 1 givenname: Amanda surname: Jimenez fullname: Jimenez, Amanda organization: Endocrinology and Diabetes Department, Obesity Unit, Hospital Clinic de Barcelona, Barcelona, Spain, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona, Spain – sequence: 2 givenname: Jordi surname: Pegueroles fullname: Pegueroles, Jordi organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 3 givenname: María surname: Carmona-Iragui fullname: Carmona-Iragui, María organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 4 givenname: Eduard surname: Vilaplana fullname: Vilaplana, Eduard organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 5 givenname: Victor surname: Montal fullname: Montal, Victor organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 6 givenname: Daniel surname: Alcolea fullname: Alcolea, Daniel organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 7 givenname: Laura surname: Videla fullname: Videla, Laura organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Barcelona Down Medical Center, Fundació Catalana de Síndrome de Down, Barcelona, Spain – sequence: 8 givenname: Ignacio surname: Illán-Gala fullname: Illán-Gala, Ignacio organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 9 givenname: Adriana surname: Pané fullname: Pané, Adriana organization: Endocrinology and Diabetes Department, Obesity Unit, Hospital Clinic de Barcelona, Barcelona, Spain – sequence: 10 givenname: Anna surname: Casajoana fullname: Casajoana, Anna organization: General Surgery Service, Hospital de Barcelona-SCIAS, Barcelona, Spain – sequence: 11 givenname: Olivia surname: Belbin fullname: Belbin, Olivia organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 12 givenname: Jordi surname: Clarimón fullname: Clarimón, Jordi organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 13 givenname: Violeta surname: Moizé fullname: Moizé, Violeta organization: Endocrinology and Diabetes Department, Obesity Unit, Hospital Clinic de Barcelona, Barcelona, Spain, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona, Spain – sequence: 14 givenname: Josep surname: Vidal fullname: Vidal, Josep organization: Endocrinology and Diabetes Department, Obesity Unit, Hospital Clinic de Barcelona, Barcelona, Spain, Institut d'Investigacions Biomèdiques August Pi Sunyer, Barcelona, Spain, Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain – sequence: 15 givenname: Alberto surname: Lleó fullname: Lleó, Alberto organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 16 givenname: Juan surname: Fortea fullname: Fortea, Juan organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain – sequence: 17 givenname: Rafael surname: Blesa fullname: Blesa, Rafael organization: Memory Unit, Department of Neurology, Hospital de la Santa Creu i Sant Pau, Biomedical Research Institute Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain, Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), San Sebastian, Spain |
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Keywords | weight loss magnetic resonance imaging Gerotarget cerebrospinal fluid Alzheimer’s disease biomarkers pre-clinical Alzheimer’s disease PET amyloid |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors share senior authorship Data used in preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wp32/content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf |
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Snippet | Weight loss has been proposed as a sign of pre-clinical Alzheimer Disease (AD). To test this hypothesis, we have evaluated the association between longitudinal... |
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Title | Weight loss in the healthy elderly might be a non-cognitive sign of preclinical Alzheimer's disease |
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