Evidence map›Paper›PMID 32588552›Full record

ArticleAnnals of clinical and translational neurology2020

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

José Rafael Romero, Serkalem Demissie, Alexa Beiser, Jayandra J Himali, Charles DeCarli, Daniel Levy, Sudha Seshadri

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

José Rafael RomeroDepartment of Neurology, Boston University School of Medicine, Boston, Massachusetts.ORCID 0000-0002-1101-2950
Serkalem DemissieDepartment of Biostatistics, Boston University School of Public Health, Boston, Massachusetts.
Alexa BeiserDepartment of Neurology, Boston University School of Medicine, Boston, Massachusetts.
Jayandra J HimaliDepartment of Neurology, Boston University School of Medicine, Boston, Massachusetts.
Charles DeCarliDepartment of Neurology, University of California- Davis, Sacramento, California.
Daniel LevyNHLBI's Framingham Heart Study, Framingham, Massachusetts.
Sudha SeshadriDepartment of Neurology, Boston University School of Medicine, Boston, Massachusetts.
Boston University · USNational Institutes of Health · USUniversity of California, Davis · US

Funding

Framingham Project/LevyZIAHL006001 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI LEVY, DANIEL · 2009 to 2025
$51.1M
UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
South Texas Alzheimer's Disease Research CenterP30AG066546 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Sudha Seshadri · 2021 to 2026
$24.0M
PRECURSORS OF STROKE INCIDENCE AND PROGNOSISR01NS017950 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Hugo Javier Aparicio, Jose Rafael Romero · 1985 to 2026
$22.9M
EPIDEMIOLOGY OF DEMENTIA IN THE FRAMINGHAM STUDYR01AG008122 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, SESHADRI, SUDHA · 1989 to 2015
$14.4M
Temporal Trends, Novel Imaging and Molecular Characterization of Preclinical and Clinical Alzheimer's Disease in the Framingham CohortsR01AG054076 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DECARLI, CHARLES, SESHADRI, SUDHA · 2016 to 2020
$12.3M
Cognitively Healthy Nonagenarians in the Cross Cohort Collaboration (CCC)RF1AG059421 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI SESHADRI, SUDHA · 2018 to 2018
$6.1M
Collaborative GWAS of Dementia, AD and related MRI and Cognitive EndophenotypesR01AG033193 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SESHADRI, SUDHA · 2009 to 2016
$4.4M
Framingham: Inflammation, Genes &Cardiovascular DiseaseR01HL076784 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BENJAMIN, EMELIA J. · 2004 to 2008
$3.9M
Aging and Inflammation: Longitudinal Markers and Genetics in the Framingham StudyR01AG028321 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BENJAMIN, EMELIA J. · 2006 to 2010
$1.8M
ADSP Follow-up in Multi-Ethnic Cohorts via Endophenotypes, Omics & Model SystemsU01AG052409 · NIA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FORNAGE, MYRIAM, SESHADRI, SUDHA · 2016 to 2020
$1.6M
Ventricular Matrix Remodeling: Correlates and PrognosisR01HL067288 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RAMACHANDRAN, VASAN S. · 2001 to 2004
$870k
NHLBI NIH HHS HHSN268201500001CNHLBI NIH HHS HHSN268201500001INHLBI NIH HHS K24 HL004334NHLBI NIH HHS R01 HL067288NHLBI NIH HHS R01 HL076784NIA NIH HHS K23 AG038444NIA NIH HHS P30 AG010129NIA NIH HHS P30 AG066546NIA NIH HHS R01 AG008122NIA NIH HHS R01 AG028321NIA NIH HHS R01 AG033193NIA NIH HHS R01 AG054076NIA NIH HHS R03 AG048180NIA NIH HHS RF1 AG059421NIA NIH HHS U01 AG052409NINDS NIH HHS R01 NS017950
6 · The paper itself

Abstract

objectiveCerebral 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.

methodsDementia, 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.

resultsCMB 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).

interpretationWe 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.

Indexed as

AdultAgedAmyloid beta-PeptidesBiomarkersCerebral HemorrhageClusterinFemaleHumansLongitudinal StudiesMaleMiddle Agedtau ProteinsAmyloid beta-PeptidesBiomarkersCLU protein, humanClusterinMAPT protein, humantau Proteins

Identifiers

PMID32588552
PMCPMC7359126
OpenAlexW3037835238

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.