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Relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study

OBJECTIVE: Cerebral microbleeds (CMBs) are associated with higher risk of stroke and dementia, predating clinical diagnosis by several years. CMB are considered markers of cerebral small vessel disease (CSVD): hypertensive (deep CMB) and cerebral amyloid angiopathy (lobar CMB). We related plasma β‐A...

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Autores principales: Romero, José Rafael, Demissie, Serkalem, Beiser, Alexa, Himali, Jayandra J., DeCarli, Charles, Levy, Daniel, Seshadri, Sudha
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7359126/
https://www.ncbi.nlm.nih.gov/pubmed/32588552
http://dx.doi.org/10.1002/acn3.51066
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author Romero, José Rafael
Demissie, Serkalem
Beiser, Alexa
Himali, Jayandra J.
DeCarli, Charles
Levy, Daniel
Seshadri, Sudha
author_facet Romero, José Rafael
Demissie, Serkalem
Beiser, Alexa
Himali, Jayandra J.
DeCarli, Charles
Levy, Daniel
Seshadri, Sudha
author_sort Romero, José Rafael
collection PubMed
description OBJECTIVE: Cerebral microbleeds (CMBs) are associated with higher risk of stroke and dementia, predating clinical diagnosis by several years. CMB are considered markers of cerebral small vessel disease (CSVD): hypertensive (deep CMB) and cerebral amyloid angiopathy (lobar CMB). We related plasma β‐Amyloid (40, 42 and their ratio), clusterin, and tau levels to CMB to elucidate their role as biomarkers for the angiopathies represented by CMB. METHODS: Dementia, stroke, and other neurological disease‐free Framingham Heart Study participants with available CMB and biomarker measurements were included. We related biomarker levels (standardized for analyses) to CMB presence overall and stratified by brain topography (any, lobar, deep), using multivariable logistic regression analyses. RESULTS: CMB were observed in 208 (5.7%) participants (mean age 57 years, 54% women). After multivariable adjustment, Aβ1‐40 was associated with any CMB (OR (95%CI) 1.20 (0.99, 1.45) P = 0.062)) and lobar CMB (OR (95%CI) 1.33 (1.05, 1.68) P = 0.019), but not with deep CMB. Log‐Aβ1‐42 levels were not associated with CMB overall. Clusterin was related to mixed CMB (1.70 [1.05, 2.74], P = 0.031). Tau levels were associated with any CMB (OR (95%CI) 1.26 (1.07, 1.49) P = 0.006), lobar CMB (OR (95%CI) 1.26 (1.05, 1.52) P = 0.013), and with deep CMB (OR (95% CI) 1.46 (1.13, 1.89) P = 0.004). INTERPRETATION: We found that plasma Aβ1‐40 and Tau are associated with CMB but further studies are needed to confirm their role in hemorrhage prone CSVD represented by CMB and as indicators of ongoing subclinical neuronal injury.
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spelling pubmed-73591262020-07-17 Relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study Romero, José Rafael Demissie, Serkalem Beiser, Alexa Himali, Jayandra J. DeCarli, Charles Levy, Daniel Seshadri, Sudha Ann Clin Transl Neurol Research Articles OBJECTIVE: Cerebral microbleeds (CMBs) are associated with higher risk of stroke and dementia, predating clinical diagnosis by several years. CMB are considered markers of cerebral small vessel disease (CSVD): hypertensive (deep CMB) and cerebral amyloid angiopathy (lobar CMB). We related plasma β‐Amyloid (40, 42 and their ratio), clusterin, and tau levels to CMB to elucidate their role as biomarkers for the angiopathies represented by CMB. METHODS: Dementia, stroke, and other neurological disease‐free Framingham Heart Study participants with available CMB and biomarker measurements were included. We related biomarker levels (standardized for analyses) to CMB presence overall and stratified by brain topography (any, lobar, deep), using multivariable logistic regression analyses. RESULTS: CMB were observed in 208 (5.7%) participants (mean age 57 years, 54% women). After multivariable adjustment, Aβ1‐40 was associated with any CMB (OR (95%CI) 1.20 (0.99, 1.45) P = 0.062)) and lobar CMB (OR (95%CI) 1.33 (1.05, 1.68) P = 0.019), but not with deep CMB. Log‐Aβ1‐42 levels were not associated with CMB overall. Clusterin was related to mixed CMB (1.70 [1.05, 2.74], P = 0.031). Tau levels were associated with any CMB (OR (95%CI) 1.26 (1.07, 1.49) P = 0.006), lobar CMB (OR (95%CI) 1.26 (1.05, 1.52) P = 0.013), and with deep CMB (OR (95% CI) 1.46 (1.13, 1.89) P = 0.004). INTERPRETATION: We found that plasma Aβ1‐40 and Tau are associated with CMB but further studies are needed to confirm their role in hemorrhage prone CSVD represented by CMB and as indicators of ongoing subclinical neuronal injury. John Wiley and Sons Inc. 2020-06-26 /pmc/articles/PMC7359126/ /pubmed/32588552 http://dx.doi.org/10.1002/acn3.51066 Text en © 2020 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Articles
Romero, José Rafael
Demissie, Serkalem
Beiser, Alexa
Himali, Jayandra J.
DeCarli, Charles
Levy, Daniel
Seshadri, Sudha
Relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study
title Relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study
title_full Relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study
title_fullStr Relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study
title_full_unstemmed Relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study
title_short Relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: Framingham Heart Study
title_sort relation of plasma β‐amyloid, clusterin, and tau with cerebral microbleeds: framingham heart study
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7359126/
https://www.ncbi.nlm.nih.gov/pubmed/32588552
http://dx.doi.org/10.1002/acn3.51066
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