Circulating IGFBP‐2: a novel biomarker for incident dementia

Objective To determine the association between plasma insulin‐like growth factor binding protein 2 (IGFBP‐2) and cognitive outcomes. Methods We measured plasma IGFBP‐2 levels in 1596 (53% women, mean age 68.7 [SD 5.7] years) dementia‐free Framingham Offspring cohort participants between 1998 and 200...

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Vydáno v:	Annals of clinical and translational neurology Ročník 6; číslo 9; s. 1659 - 1670
Hlavní autoři:	McGrath, Emer R., Himali, Jayandra J., Levy, Daniel, Conner, Sarah C., DeCarli, Charles S., Pase, Matthew P., Courchesne, Paul, Satizabal, Claudia L., Vasan, Ramachandran S., Beiser, Alexa S., Seshadri, Sudha
Médium:	Journal Article
Jazyk:	angličtina
Vydáno:	United States John Wiley & Sons, Inc 01.09.2019 John Wiley and Sons Inc Wiley
Témata:	Aged Alzheimer Disease - blood Alzheimer Disease - diagnosis Alzheimer Disease - epidemiology Alzheimer's disease Biomarkers Biomarkers - blood Cognitive ability Dementia Dementia - blood Dementia - diagnosis Dementia - epidemiology Female Growth factors Humans Incidence Insulin resistance Insulin-Like Growth Factor Binding Protein 3 - blood Male Metabolism Middle Aged NMR Nuclear magnetic resonance Probability Prospective Studies Proteins Risk
ISSN:	2328-9503, 2328-9503
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Abstract	Objective To determine the association between plasma insulin‐like growth factor binding protein 2 (IGFBP‐2) and cognitive outcomes. Methods We measured plasma IGFBP‐2 levels in 1596 (53% women, mean age 68.7 [SD 5.7] years) dementia‐free Framingham Offspring cohort participants between 1998 and 2001. Multivariable Cox proportional hazards models related plasma IGFBP‐2 to subsequent risk of incident dementia and Alzheimer’s disease. MRI brain measures and cognitive performance were included as secondary outcomes. Results During a median follow‐up of 11.8 (Q1, Q3: 7.1, 13.3) years, 131 participants developed incident dementia, of whom 98 were diagnosed with Alzheimer’s disease. The highest tertile of IGFBP‐2, compared to the lowest tertile, was associated with an increased risk of incident all‐cause dementia (hazard ratio [HR] 2.89, 95% CI 1.63–5.13) and Alzheimer’s disease (HR 3.63, 95% CI 1.76–7.50) in multivariable analysis. Higher circulating IGFBP2 levels were also cross‐sectionally associated with poorer performance on tests of reasoning but not with MRI‐based outcomes. After adding plasma IGFBP‐2 levels to a conventional dementia prediction model, 32% of individuals with dementia were correctly assigned a higher predicted risk, while 8% of individuals without dementia were correctly assigned a lower predicted risk (overall net reclassification improvement index, 0.40, 95% CI 0.22–0.59). Interpretation Elevated circulating IGFBP‐2 levels were associated with an increased risk of both all‐cause dementia and Alzheimer’s disease. Addition of IGFBP2 plasma levels to a model of traditional risk factors significantly improved dementia risk classification. Manipulation of insulin‐like growth factor signaling via IGFBP‐2 may be a promising therapeutic target for dementia.
AbstractList	To determine the association between plasma insulin-like growth factor binding protein 2 (IGFBP-2) and cognitive outcomes.OBJECTIVETo determine the association between plasma insulin-like growth factor binding protein 2 (IGFBP-2) and cognitive outcomes.We measured plasma IGFBP-2 levels in 1596 (53% women, mean age 68.7 [SD 5.7] years) dementia-free Framingham Offspring cohort participants between 1998 and 2001. Multivariable Cox proportional hazards models related plasma IGFBP-2 to subsequent risk of incident dementia and Alzheimer's disease. MRI brain measures and cognitive performance were included as secondary outcomes.METHODSWe measured plasma IGFBP-2 levels in 1596 (53% women, mean age 68.7 [SD 5.7] years) dementia-free Framingham Offspring cohort participants between 1998 and 2001. Multivariable Cox proportional hazards models related plasma IGFBP-2 to subsequent risk of incident dementia and Alzheimer's disease. MRI brain measures and cognitive performance were included as secondary outcomes.During a median follow-up of 11.8 (Q1, Q3: 7.1, 13.3) years, 131 participants developed incident dementia, of whom 98 were diagnosed with Alzheimer's disease. The highest tertile of IGFBP-2, compared to the lowest tertile, was associated with an increased risk of incident all-cause dementia (hazard ratio [HR] 2.89, 95% CI 1.63-5.13) and Alzheimer's disease (HR 3.63, 95% CI 1.76-7.50) in multivariable analysis. Higher circulating IGFBP2 levels were also cross-sectionally associated with poorer performance on tests of abstract reasoning but not with MRI-based outcomes. After adding plasma IGFBP-2 levels to a conventional dementia prediction model, 32% of individuals with dementia were correctly assigned a higher predicted risk, while 8% of individuals without dementia were correctly assigned a lower predicted risk (overall net reclassification improvement index, 0.40, 95% CI 0.22-0.59).RESULTSDuring a median follow-up of 11.8 (Q1, Q3: 7.1, 13.3) years, 131 participants developed incident dementia, of whom 98 were diagnosed with Alzheimer's disease. The highest tertile of IGFBP-2, compared to the lowest tertile, was associated with an increased risk of incident all-cause dementia (hazard ratio [HR] 2.89, 95% CI 1.63-5.13) and Alzheimer's disease (HR 3.63, 95% CI 1.76-7.50) in multivariable analysis. Higher circulating IGFBP2 levels were also cross-sectionally associated with poorer performance on tests of abstract reasoning but not with MRI-based outcomes. After adding plasma IGFBP-2 levels to a conventional dementia prediction model, 32% of individuals with dementia were correctly assigned a higher predicted risk, while 8% of individuals without dementia were correctly assigned a lower predicted risk (overall net reclassification improvement index, 0.40, 95% CI 0.22-0.59).Elevated circulating IGFBP-2 levels were associated with an increased risk of both all-cause dementia and Alzheimer's disease. Addition of IGFBP2 plasma levels to a model of traditional risk factors significantly improved dementia risk classification. Manipulation of insulin-like growth factor signaling via IGFBP-2 may be a promising therapeutic target for dementia.INTERPRETATIONElevated circulating IGFBP-2 levels were associated with an increased risk of both all-cause dementia and Alzheimer's disease. Addition of IGFBP2 plasma levels to a model of traditional risk factors significantly improved dementia risk classification. Manipulation of insulin-like growth factor signaling via IGFBP-2 may be a promising therapeutic target for dementia. Abstract Objective To determine the association between plasma insulin‐like growth factor binding protein 2 (IGFBP‐2) and cognitive outcomes. Methods We measured plasma IGFBP‐2 levels in 1596 (53% women, mean age 68.7 [SD 5.7] years) dementia‐free Framingham Offspring cohort participants between 1998 and 2001. Multivariable Cox proportional hazards models related plasma IGFBP‐2 to subsequent risk of incident dementia and Alzheimer’s disease. MRI brain measures and cognitive performance were included as secondary outcomes. Results During a median follow‐up of 11.8 (Q1, Q3: 7.1, 13.3) years, 131 participants developed incident dementia, of whom 98 were diagnosed with Alzheimer’s disease. The highest tertile of IGFBP‐2, compared to the lowest tertile, was associated with an increased risk of incident all‐cause dementia (hazard ratio [HR] 2.89, 95% CI 1.63–5.13) and Alzheimer’s disease (HR 3.63, 95% CI 1.76–7.50) in multivariable analysis. Higher circulating IGFBP2 levels were also cross‐sectionally associated with poorer performance on tests of abstract reasoning but not with MRI‐based outcomes. After adding plasma IGFBP‐2 levels to a conventional dementia prediction model, 32% of individuals with dementia were correctly assigned a higher predicted risk, while 8% of individuals without dementia were correctly assigned a lower predicted risk (overall net reclassification improvement index, 0.40, 95% CI 0.22–0.59). Interpretation Elevated circulating IGFBP‐2 levels were associated with an increased risk of both all‐cause dementia and Alzheimer’s disease. Addition of IGFBP2 plasma levels to a model of traditional risk factors significantly improved dementia risk classification. Manipulation of insulin‐like growth factor signaling via IGFBP‐2 may be a promising therapeutic target for dementia. Objective To determine the association between plasma insulin‐like growth factor binding protein 2 (IGFBP‐2) and cognitive outcomes. Methods We measured plasma IGFBP‐2 levels in 1596 (53% women, mean age 68.7 [SD 5.7] years) dementia‐free Framingham Offspring cohort participants between 1998 and 2001. Multivariable Cox proportional hazards models related plasma IGFBP‐2 to subsequent risk of incident dementia and Alzheimer’s disease. MRI brain measures and cognitive performance were included as secondary outcomes. Results During a median follow‐up of 11.8 (Q1, Q3: 7.1, 13.3) years, 131 participants developed incident dementia, of whom 98 were diagnosed with Alzheimer’s disease. The highest tertile of IGFBP‐2, compared to the lowest tertile, was associated with an increased risk of incident all‐cause dementia (hazard ratio [HR] 2.89, 95% CI 1.63–5.13) and Alzheimer’s disease (HR 3.63, 95% CI 1.76–7.50) in multivariable analysis. Higher circulating IGFBP2 levels were also cross‐sectionally associated with poorer performance on tests of reasoning but not with MRI‐based outcomes. After adding plasma IGFBP‐2 levels to a conventional dementia prediction model, 32% of individuals with dementia were correctly assigned a higher predicted risk, while 8% of individuals without dementia were correctly assigned a lower predicted risk (overall net reclassification improvement index, 0.40, 95% CI 0.22–0.59). Interpretation Elevated circulating IGFBP‐2 levels were associated with an increased risk of both all‐cause dementia and Alzheimer’s disease. Addition of IGFBP2 plasma levels to a model of traditional risk factors significantly improved dementia risk classification. Manipulation of insulin‐like growth factor signaling via IGFBP‐2 may be a promising therapeutic target for dementia. To determine the association between plasma insulin-like growth factor binding protein 2 (IGFBP-2) and cognitive outcomes. We measured plasma IGFBP-2 levels in 1596 (53% women, mean age 68.7 [SD 5.7] years) dementia-free Framingham Offspring cohort participants between 1998 and 2001. Multivariable Cox proportional hazards models related plasma IGFBP-2 to subsequent risk of incident dementia and Alzheimer's disease. MRI brain measures and cognitive performance were included as secondary outcomes. During a median follow-up of 11.8 (Q1, Q3: 7.1, 13.3) years, 131 participants developed incident dementia, of whom 98 were diagnosed with Alzheimer's disease. The highest tertile of IGFBP-2, compared to the lowest tertile, was associated with an increased risk of incident all-cause dementia (hazard ratio [HR] 2.89, 95% CI 1.63-5.13) and Alzheimer's disease (HR 3.63, 95% CI 1.76-7.50) in multivariable analysis. Higher circulating IGFBP2 levels were also cross-sectionally associated with poorer performance on tests of abstract reasoning but not with MRI-based outcomes. After adding plasma IGFBP-2 levels to a conventional dementia prediction model, 32% of individuals with dementia were correctly assigned a higher predicted risk, while 8% of individuals without dementia were correctly assigned a lower predicted risk (overall net reclassification improvement index, 0.40, 95% CI 0.22-0.59). Elevated circulating IGFBP-2 levels were associated with an increased risk of both all-cause dementia and Alzheimer's disease. Addition of IGFBP2 plasma levels to a model of traditional risk factors significantly improved dementia risk classification. Manipulation of insulin-like growth factor signaling via IGFBP-2 may be a promising therapeutic target for dementia. ObjectiveTo determine the association between plasma insulin‐like growth factor binding protein 2 (IGFBP‐2) and cognitive outcomes.MethodsWe measured plasma IGFBP‐2 levels in 1596 (53% women, mean age 68.7 [SD 5.7] years) dementia‐free Framingham Offspring cohort participants between 1998 and 2001. Multivariable Cox proportional hazards models related plasma IGFBP‐2 to subsequent risk of incident dementia and Alzheimer’s disease. MRI brain measures and cognitive performance were included as secondary outcomes.ResultsDuring a median follow‐up of 11.8 (Q1, Q3: 7.1, 13.3) years, 131 participants developed incident dementia, of whom 98 were diagnosed with Alzheimer’s disease. The highest tertile of IGFBP‐2, compared to the lowest tertile, was associated with an increased risk of incident all‐cause dementia (hazard ratio [HR] 2.89, 95% CI 1.63–5.13) and Alzheimer’s disease (HR 3.63, 95% CI 1.76–7.50) in multivariable analysis. Higher circulating IGFBP2 levels were also cross‐sectionally associated with poorer performance on tests of abstract reasoning but not with MRI‐based outcomes. After adding plasma IGFBP‐2 levels to a conventional dementia prediction model, 32% of individuals with dementia were correctly assigned a higher predicted risk, while 8% of individuals without dementia were correctly assigned a lower predicted risk (overall net reclassification improvement index, 0.40, 95% CI 0.22–0.59).InterpretationElevated circulating IGFBP‐2 levels were associated with an increased risk of both all‐cause dementia and Alzheimer’s disease. Addition of IGFBP2 plasma levels to a model of traditional risk factors significantly improved dementia risk classification. Manipulation of insulin‐like growth factor signaling via IGFBP‐2 may be a promising therapeutic target for dementia.
Author	Himali, Jayandra J. DeCarli, Charles S. Vasan, Ramachandran S. Courchesne, Paul Levy, Daniel Pase, Matthew P. McGrath, Emer R. Seshadri, Sudha Conner, Sarah C. Satizabal, Claudia L. Beiser, Alexa S.
AuthorAffiliation	2 Harvard Medical School Boston Massachusetts 1 Department of Neurology Brigham & Women’s Hospital Boston Massachusetts 10 Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases University of Texas Health Sciences Center San Antonio Texas 6 Population Sciences Branch of the National Heart, Lung, Blood Institute of the National Institutes of Health Bethesda Maryland 8 Melbourne Dementia Research Centre The Florey Institute for Neuroscience and Mental Health Melbourne Victoria Australia 4 Boston University School of Public Health Boston Massachusetts 5 Boston University School of Medicine Boston Massachusetts 3 Framingham Heart Study Framingham Massachusetts 9 University of Melbourne Melbourne Victoria Australia 7 Department of Neurology University of California Davis California
AuthorAffiliation_xml	– name: 3 Framingham Heart Study Framingham Massachusetts – name: 4 Boston University School of Public Health Boston Massachusetts – name: 7 Department of Neurology University of California Davis California – name: 6 Population Sciences Branch of the National Heart, Lung, Blood Institute of the National Institutes of Health Bethesda Maryland – name: 1 Department of Neurology Brigham & Women’s Hospital Boston Massachusetts – name: 9 University of Melbourne Melbourne Victoria Australia – name: 2 Harvard Medical School Boston Massachusetts – name: 8 Melbourne Dementia Research Centre The Florey Institute for Neuroscience and Mental Health Melbourne Victoria Australia – name: 5 Boston University School of Medicine Boston Massachusetts – name: 10 Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases University of Texas Health Sciences Center San Antonio Texas
Author_xml	– sequence: 1 givenname: Emer R. orcidid: 0000-0002-3589-2964 surname: McGrath fullname: McGrath, Emer R. email: emcgrath2@bwh.harvard.edu organization: Framingham Heart Study – sequence: 2 givenname: Jayandra J. surname: Himali fullname: Himali, Jayandra J. organization: Boston University School of Medicine – sequence: 3 givenname: Daniel surname: Levy fullname: Levy, Daniel organization: Population Sciences Branch of the National Heart, Lung, Blood Institute of the National Institutes of Health – sequence: 4 givenname: Sarah C. orcidid: 0000-0002-0929-9948 surname: Conner fullname: Conner, Sarah C. organization: Boston University School of Public Health – sequence: 5 givenname: Charles S. surname: DeCarli fullname: DeCarli, Charles S. organization: University of California – sequence: 6 givenname: Matthew P. surname: Pase fullname: Pase, Matthew P. organization: University of Melbourne – sequence: 7 givenname: Paul surname: Courchesne fullname: Courchesne, Paul organization: Population Sciences Branch of the National Heart, Lung, Blood Institute of the National Institutes of Health – sequence: 8 givenname: Claudia L. surname: Satizabal fullname: Satizabal, Claudia L. organization: University of Texas Health Sciences Center – sequence: 9 givenname: Ramachandran S. surname: Vasan fullname: Vasan, Ramachandran S. organization: Boston University School of Medicine – sequence: 10 givenname: Alexa S. surname: Beiser fullname: Beiser, Alexa S. organization: Boston University School of Medicine – sequence: 11 givenname: Sudha surname: Seshadri fullname: Seshadri, Sudha organization: University of Texas Health Sciences Center
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/31373442$$D View this record in MEDLINE/PubMed
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License	Attribution-NonCommercial-NoDerivs 2019 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc. on behalf of American Neurological Association. This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
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Notes	The Framingham Heart Study is supported by the National Heart, Lung, and Blood Institute (contract no. N01‐HC‐25195 and no. HHSN268201500001I). This research was supported by an Alzheimer’s Association Clinician Scientist Fellowship (AACSF‐18‐566570), NHLBI grants R01 HL60040 and R01 HL70100, grants from the National Institute on Aging (R01 AG054076, R01 AG049607, R01 AG033193, U01 AG049505, U01 AG052409), and grants from the National Institute of Neurological Disorders and Stroke (NS017950 and UH2 NS100605). Additional funding for the Systems Approach to Biomarker Research in Cardiovascular Disease (SABRe CVD) initiative was provided by the Division of Intramural Research, NHLBI, and the Population Sciences Branch, NHLBI. MPP is funded by a National Heart Foundation of Australia Future Leader Fellowship (102052). SCC is funded by the National Institute of General Medical Sciences (NIGMS) Interdisciplinary Training Grant for Biostatisticians (T32GM74905‐14). None of the funding entities had any role in the design and conduct of the study; collection, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; or decision to submit the manuscript for publication. The views and opinions offered in this manuscript are those of the authors and are not necessarily those of the funding agencies. Funding Information ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23
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Snippet	Objective To determine the association between plasma insulin‐like growth factor binding protein 2 (IGFBP‐2) and cognitive outcomes. Methods We measured plasma... To determine the association between plasma insulin-like growth factor binding protein 2 (IGFBP-2) and cognitive outcomes. We measured plasma IGFBP-2 levels in... ObjectiveTo determine the association between plasma insulin‐like growth factor binding protein 2 (IGFBP‐2) and cognitive outcomes.MethodsWe measured plasma... To determine the association between plasma insulin-like growth factor binding protein 2 (IGFBP-2) and cognitive outcomes.OBJECTIVETo determine the association... Abstract Objective To determine the association between plasma insulin‐like growth factor binding protein 2 (IGFBP‐2) and cognitive outcomes. Methods We...
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SubjectTerms	Aged Alzheimer Disease - blood Alzheimer Disease - diagnosis Alzheimer Disease - epidemiology Alzheimer's disease Biomarkers Biomarkers - blood Cognitive ability Dementia Dementia - blood Dementia - diagnosis Dementia - epidemiology Female Growth factors Humans Incidence Insulin resistance Insulin-Like Growth Factor Binding Protein 3 - blood Male Metabolism Middle Aged NMR Nuclear magnetic resonance Probability Prospective Studies Proteins Risk
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Title	Circulating IGFBP‐2: a novel biomarker for incident dementia
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