Growth Differentiation Factor 15 and NT‐proBNP as Blood‐Based Markers of Vascular Brain Injury and Dementia

Background GDF15 (growth differentiation factor 15) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) may offer promise as biomarkers for cognitive outcomes, including dementia. We determined the association of these biomarkers with cognitive outcomes in a community-based cohort. Methods and...

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Published in:	Journal of the American Heart Association Vol. 9; no. 19; p. e014659
Main Authors:	McGrath, Emer R., Himali, Jayandra J., Levy, Daniel, Conner, Sarah C., DeCarli, Charles, Pase, Matthew P., Ninomiya, Toshiharu, Ohara, Tomoyuki, Courchesne, Paul, Satizabal, Claudia L., Vasan, Ramachandran S., Beiser, Alexa S., Seshadri, Sudha
Format:	Journal Article
Language:	English
Published:	England John Wiley and Sons Inc 20.10.2020 Wiley
Subjects:	Aged biomarker Biomarkers - blood Cerebrovascular Trauma - blood Cerebrovascular Trauma - diagnostic imaging dementia Dementia - blood Dementia - diagnostic imaging Female Growth Differentiation Factor 15 - blood Humans Magnetic Resonance Imaging Male Natriuretic Peptide, Brain - blood Neuroimaging Original Research Peptide Fragments - blood Proportional Hazards Models Prospective Studies vascular cognitive impairment vascular cognitive impairment biomarker dementia
ISSN:	2047-9980, 2047-9980
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Abstract	Background GDF15 (growth differentiation factor 15) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) may offer promise as biomarkers for cognitive outcomes, including dementia. We determined the association of these biomarkers with cognitive outcomes in a community-based cohort. Methods and Results Plasma GDF15 (n=1603) and NT-proBNP levels (n=1590) (53% women; mean age, 68.7 years) were measured in dementia-free Framingham Offspring cohort participants at examination 7 (1998-2001). Participants were followed up for incident dementia. Secondary outcomes included Alzheimer disease dementia, magnetic resonance imaging structural brain measures, and neurocognitive performance. During a median 11.8-year follow-up, 131 participants developed dementia. On multivariable Cox proportional-hazards analysis, higher circulating GDF15 was associated with an increased risk of incident all-cause and Alzheimer disease dementia (hazard ratio [HR] per SD increment in natural log-transformed biomarker value, 1.54 [95% CI, 1.22-1.95] and 1.37 [95% CI, 1.03-1.81], respectively), whereas higher plasma NT-proBNP was also associated with an increased risk of all-cause dementia (HR, 1.32; 95% CI, 1.05-1.65). Elevated GDF15 was associated with lower total brain and hippocampal volumes, greater white matter hyperintensity volume, and poorer cognitive performance. Elevated NT-proBNP was associated with greater white matter hyperintensity volume and poorer cognitive performance. Addition of both biomarkers to a conventional risk factor model improved dementia risk classification (net reclassification improvement index, 0.25; 95% CI, 0.05-0.45). Conclusions Elevated plasma GDF15 and NT-proBNP were associated with vascular brain injury on magnetic resonance imaging, poorer neurocognitive performance, and increased risk of incident dementia in individuals aged >60 years. Both biomarkers improved dementia risk classification beyond that of traditional clinical risk factors, indicating their potential value in predicting incident dementia.
AbstractList	Background GDF15 (growth differentiation factor 15) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) may offer promise as biomarkers for cognitive outcomes, including dementia. We determined the association of these biomarkers with cognitive outcomes in a community-based cohort. Methods and Results Plasma GDF15 (n=1603) and NT-proBNP levels (n=1590) (53% women; mean age, 68.7 years) were measured in dementia-free Framingham Offspring cohort participants at examination 7 (1998-2001). Participants were followed up for incident dementia. Secondary outcomes included Alzheimer disease dementia, magnetic resonance imaging structural brain measures, and neurocognitive performance. During a median 11.8-year follow-up, 131 participants developed dementia. On multivariable Cox proportional-hazards analysis, higher circulating GDF15 was associated with an increased risk of incident all-cause and Alzheimer disease dementia (hazard ratio [HR] per SD increment in natural log-transformed biomarker value, 1.54 [95% CI, 1.22-1.95] and 1.37 [95% CI, 1.03-1.81], respectively), whereas higher plasma NT-proBNP was also associated with an increased risk of all-cause dementia (HR, 1.32; 95% CI, 1.05-1.65). Elevated GDF15 was associated with lower total brain and hippocampal volumes, greater white matter hyperintensity volume, and poorer cognitive performance. Elevated NT-proBNP was associated with greater white matter hyperintensity volume and poorer cognitive performance. Addition of both biomarkers to a conventional risk factor model improved dementia risk classification (net reclassification improvement index, 0.25; 95% CI, 0.05-0.45). Conclusions Elevated plasma GDF15 and NT-proBNP were associated with vascular brain injury on magnetic resonance imaging, poorer neurocognitive performance, and increased risk of incident dementia in individuals aged >60 years. Both biomarkers improved dementia risk classification beyond that of traditional clinical risk factors, indicating their potential value in predicting incident dementia.Background GDF15 (growth differentiation factor 15) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) may offer promise as biomarkers for cognitive outcomes, including dementia. We determined the association of these biomarkers with cognitive outcomes in a community-based cohort. Methods and Results Plasma GDF15 (n=1603) and NT-proBNP levels (n=1590) (53% women; mean age, 68.7 years) were measured in dementia-free Framingham Offspring cohort participants at examination 7 (1998-2001). Participants were followed up for incident dementia. Secondary outcomes included Alzheimer disease dementia, magnetic resonance imaging structural brain measures, and neurocognitive performance. During a median 11.8-year follow-up, 131 participants developed dementia. On multivariable Cox proportional-hazards analysis, higher circulating GDF15 was associated with an increased risk of incident all-cause and Alzheimer disease dementia (hazard ratio [HR] per SD increment in natural log-transformed biomarker value, 1.54 [95% CI, 1.22-1.95] and 1.37 [95% CI, 1.03-1.81], respectively), whereas higher plasma NT-proBNP was also associated with an increased risk of all-cause dementia (HR, 1.32; 95% CI, 1.05-1.65). Elevated GDF15 was associated with lower total brain and hippocampal volumes, greater white matter hyperintensity volume, and poorer cognitive performance. Elevated NT-proBNP was associated with greater white matter hyperintensity volume and poorer cognitive performance. Addition of both biomarkers to a conventional risk factor model improved dementia risk classification (net reclassification improvement index, 0.25; 95% CI, 0.05-0.45). Conclusions Elevated plasma GDF15 and NT-proBNP were associated with vascular brain injury on magnetic resonance imaging, poorer neurocognitive performance, and increased risk of incident dementia in individuals aged >60 years. Both biomarkers improved dementia risk classification beyond that of traditional clinical risk factors, indicating their potential value in predicting incident dementia. Background GDF15 (growth differentiation factor 15) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) may offer promise as biomarkers for cognitive outcomes, including dementia. We determined the association of these biomarkers with cognitive outcomes in a community-based cohort. Methods and Results Plasma GDF15 (n=1603) and NT-proBNP levels (n=1590) (53% women; mean age, 68.7 years) were measured in dementia-free Framingham Offspring cohort participants at examination 7 (1998-2001). Participants were followed up for incident dementia. Secondary outcomes included Alzheimer disease dementia, magnetic resonance imaging structural brain measures, and neurocognitive performance. During a median 11.8-year follow-up, 131 participants developed dementia. On multivariable Cox proportional-hazards analysis, higher circulating GDF15 was associated with an increased risk of incident all-cause and Alzheimer disease dementia (hazard ratio [HR] per SD increment in natural log-transformed biomarker value, 1.54 [95% CI, 1.22-1.95] and 1.37 [95% CI, 1.03-1.81], respectively), whereas higher plasma NT-proBNP was also associated with an increased risk of all-cause dementia (HR, 1.32; 95% CI, 1.05-1.65). Elevated GDF15 was associated with lower total brain and hippocampal volumes, greater white matter hyperintensity volume, and poorer cognitive performance. Elevated NT-proBNP was associated with greater white matter hyperintensity volume and poorer cognitive performance. Addition of both biomarkers to a conventional risk factor model improved dementia risk classification (net reclassification improvement index, 0.25; 95% CI, 0.05-0.45). Conclusions Elevated plasma GDF15 and NT-proBNP were associated with vascular brain injury on magnetic resonance imaging, poorer neurocognitive performance, and increased risk of incident dementia in individuals aged >60 years. Both biomarkers improved dementia risk classification beyond that of traditional clinical risk factors, indicating their potential value in predicting incident dementia.
Author	Himali, Jayandra J. Vasan, Ramachandran S. Courchesne, Paul DeCarli, Charles Pase, Matthew P. McGrath, Emer R. Seshadri, Sudha Ninomiya, Toshiharu Satizabal, Claudia L. Beiser, Alexa S. Ohara, Tomoyuki Levy, Daniel Conner, Sarah C.
AuthorAffiliation	9 Harvard University Boston MA Australia 6 Population Sciences Branch National Heart, Lung, and Blood Institutes of Health Bethesda MD 7 Department of Neurology University of California Davis CA 1 HRB Clinical Research Facility National University of Ireland Galway Galway Ireland 2 Framingham Heart Study Framingham MA 4 Boston University School of Medicine Boston MA 5 Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases University of Texas Health Sciences Center San Antonio TX 3 Boston University School of Public Health Boston MA 8 Turner Institute Monash University Clayton Victoria Australia 10 Department of Epidemiology and Public Health Graduate School of Medical Sciences Kyushu University Fukuoka Japan
AuthorAffiliation_xml	– name: 1 HRB Clinical Research Facility National University of Ireland Galway Galway Ireland – name: 2 Framingham Heart Study Framingham MA – name: 7 Department of Neurology University of California Davis CA – name: 8 Turner Institute Monash University Clayton Victoria Australia – name: 10 Department of Epidemiology and Public Health Graduate School of Medical Sciences Kyushu University Fukuoka Japan – name: 4 Boston University School of Medicine Boston MA – name: 5 Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases University of Texas Health Sciences Center San Antonio TX – name: 9 Harvard University Boston MA Australia – name: 3 Boston University School of Public Health Boston MA – name: 6 Population Sciences Branch National Heart, Lung, and Blood Institutes of Health Bethesda MD
Author_xml	– sequence: 1 givenname: Emer R. orcidid: 0000-0002-3589-2964 surname: McGrath fullname: McGrath, Emer R. organization: HRB Clinical Research Facility National University of Ireland Galway Galway Ireland, Framingham Heart Study Framingham MA – sequence: 2 givenname: Jayandra J. surname: Himali fullname: Himali, Jayandra J. organization: Framingham Heart Study Framingham MA, Boston University School of Public Health Boston MA, Boston University School of Medicine Boston MA, Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases University of Texas Health Sciences Center San Antonio TX – sequence: 3 givenname: Daniel surname: Levy fullname: Levy, Daniel organization: Framingham Heart Study Framingham MA, Population Sciences Branch National Heart, Lung, and Blood Institutes of Health Bethesda MD – sequence: 4 givenname: Sarah C. orcidid: 0000-0002-0929-9948 surname: Conner fullname: Conner, Sarah C. organization: Framingham Heart Study Framingham MA, Boston University School of Medicine Boston MA – sequence: 5 givenname: Charles surname: DeCarli fullname: DeCarli, Charles organization: Department of Neurology University of California Davis CA – sequence: 6 givenname: Matthew P. surname: Pase fullname: Pase, Matthew P. organization: Framingham Heart Study Framingham MA, Turner Institute Monash University Clayton Victoria Australia, Harvard University Boston MA Australia – sequence: 7 givenname: Toshiharu surname: Ninomiya fullname: Ninomiya, Toshiharu organization: Department of Epidemiology and Public Health Graduate School of Medical Sciences Kyushu University Fukuoka Japan – sequence: 8 givenname: Tomoyuki surname: Ohara fullname: Ohara, Tomoyuki organization: Department of Epidemiology and Public Health Graduate School of Medical Sciences Kyushu University Fukuoka Japan – sequence: 9 givenname: Paul surname: Courchesne fullname: Courchesne, Paul organization: Framingham Heart Study Framingham MA – sequence: 10 givenname: Claudia L. orcidid: 0000-0002-1115-4430 surname: Satizabal fullname: Satizabal, Claudia L. organization: Framingham Heart Study Framingham MA, Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases University of Texas Health Sciences Center San Antonio TX – sequence: 11 givenname: Ramachandran S. orcidid: 0000-0001-7357-5970 surname: Vasan fullname: Vasan, Ramachandran S. organization: Framingham Heart Study Framingham MA, Boston University School of Medicine Boston MA – sequence: 12 givenname: Alexa S. orcidid: 0000-0001-8551-7778 surname: Beiser fullname: Beiser, Alexa S. organization: Framingham Heart Study Framingham MA, Boston University School of Public Health Boston MA, Boston University School of Medicine Boston MA – sequence: 13 givenname: Sudha surname: Seshadri fullname: Seshadri, Sudha organization: Framingham Heart Study Framingham MA, Boston University School of Medicine Boston MA, Glenn Biggs Institute for Alzheimer’s & Neurodegenerative Diseases University of Texas Health Sciences Center San Antonio TX
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Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Current address: Turner Institute, Monash University, Clayton, Victoria, Australia and Harvard University, Boston, MA.For Sources of Funding and Disclosures, see page 9. Supplementary materials for this article are available at https://www.ahajournals.org/doi/suppl/10.1161/JAHA.119.014659
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Snippet	Background GDF15 (growth differentiation factor 15) and NT-proBNP (N-terminal pro-B-type natriuretic peptide) may offer promise as biomarkers for cognitive... Background GDF15 (growth differentiation factor 15) and NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide) may offer promise as biomarkers for cognitive...
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SubjectTerms	Aged biomarker Biomarkers - blood Cerebrovascular Trauma - blood Cerebrovascular Trauma - diagnostic imaging dementia Dementia - blood Dementia - diagnostic imaging Female Growth Differentiation Factor 15 - blood Humans Magnetic Resonance Imaging Male Natriuretic Peptide, Brain - blood Neuroimaging Original Research Peptide Fragments - blood Proportional Hazards Models Prospective Studies vascular cognitive impairment
Title	Growth Differentiation Factor 15 and NT‐proBNP as Blood‐Based Markers of Vascular Brain Injury and Dementia
URI	https://www.ncbi.nlm.nih.gov/pubmed/32921207 https://www.proquest.com/docview/2442599255 https://pubmed.ncbi.nlm.nih.gov/PMC7792414 https://doaj.org/article/af8ae7f41abc4647a1432a7d44464840
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