Evidence map›Paper›PMID 33720897›Full record

ArticleJournal of Alzheimer's disease : JAD2021

Cerebral Amyloid Angiopathy Burden and Cerebral Microbleeds: Pathological Evidence for Distinct Phenotypes.

Jonathan Graff-Radford, Timothy G Lesnick, Michelle M Mielke, Eleni Constantopoulos, Alejandro A Rabinstein, Scott A Przybelski, Prashanthi Vemuri, Hugo Botha, David T Jones, Vijay K Ramanan and 8 more

Open access · greenAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 15 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

18 authors at 3 institutions in 1 country.

Jonathan Graff-RadfordDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Timothy G LesnickDepartment of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
Michelle M MielkeDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Eleni ConstantopoulosDepartment of Pathology and Laboratory Medicine, Mayo Clinic, Rochester, MN, USA.
Alejandro A RabinsteinDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Scott A PrzybelskiDepartment of Health Sciences Research, Mayo Clinic, Rochester, MN, USA.
Prashanthi VemuriDepartment of Radiology, Mayo Clinic, Rochester, MN, USA.
Hugo BothaDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
David T JonesDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Vijay K RamananDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Ronald C PetersenDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
David S KnopmanDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Bradley F BoeveDepartment of Neurology, Mayo Clinic, Rochester, MN, USA.
Melissa E MurrayDepartment of Pathology and Laboratory Medicine, Mayo Clinic, Jacksonville, FL, USA.
Dennis W DicksonDepartment of Pathology and Laboratory Medicine, Mayo Clinic, Jacksonville, FL, USA.
Clifford R JackDepartment of Radiology, Mayo Clinic, Rochester, MN, USA.
Kejal KantarciDepartment of Radiology, Mayo Clinic, Rochester, MN, USA.
R Ross ReichardDepartment of Pathology and Laboratory Medicine, Mayo Clinic, Rochester, MN, USA.
Mayo Clinic in Arizona · USMayo Clinic in Florida · USWinnMed · US

Funding

SUPPLEMENT TO ALZHEIMERS DISEASE PATIENT REGISTRYU01AG006786 · NIA · MAYO CLINIC ROCHESTER · PI GRAFF-RADFORD, JONATHAN, JACK, CLIFFORD R. · 1986 to 2023
$49.6M
THE PGRN/TDP-43 AXIS IN ALZHEIMER?S DISEASE AND NEURODEGENERATIONP50AG016574 · NIA · MAYO CLINIC ROCHESTER · PI BU, GUOJUN · 1999 to 2018
$36.9M
Research Education ComponentP30AG062677 · NIA · MAYO CLINIC ROCHESTER · PI DAVID S KNOPMAN · 2019 to 2026
$33.5M
PREDICTING ALZHEIMERS DISEASE WITH MAGNETIC RESONANCER01AG011378 · NIA · MAYO CLINIC ROCHESTER · PI JACK, CLIFFORD R. · 1993 to 2017
$12.1M
Investigating Resistance and Resilience Mechanisms in Alzheimer’s DiseaseR01AG056366 · NIA · MAYO CLINIC ROCHESTER · PI PRASHANTHI VEMURI · 2017 to 2026
$7.0M
Disease pathways in the population determined by amyloid, tau, and neurodegeneration imaging biomarkersR37AG011378 · NIA · MAYO CLINIC ROCHESTER · PI CLIFFORD R. JACK · 2018 to 2026
$6.8M
Development, Validation, and Application of an Imaging based CVD ScaleR01NS097495 · NINDS · MAYO CLINIC ROCHESTER · PI VEMURI, PRASHANTHI · 2016 to 2020
$2.9M
Cerebral Microbleeds in the Aging PopulationK76AG057015 · NIA · MAYO CLINIC ROCHESTER · PI GRAFF-RADFORD, JONATHAN · 2017 to 2021
$1.2M
NIA NIH HHS K76 AG057015NIA NIH HHS P30 AG062677NIA NIH HHS P50 AG016574NIA NIH HHS R01 AG011378NIA NIH HHS R01 AG056366NIA NIH HHS R37 AG011378NIA NIH HHS U01 AG006786NINDS NIH HHS R01 NS097495
6 · The paper itself

Abstract

backgroundThe relationship between cerebral microbleeds (CMBs) on hemosiderin-sensitive MRI sequences and cerebral amyloid angiopathy (CAA) remains unclear in population-based participants or in individuals with dementia.

objectiveTo determine whether CMBs on antemortem MRI correlate with CAA.

methodsWe reviewed 54 consecutive participants with antemortem T2*GRE-MRI sequences and subsequent autopsy. CMBs were quantified on MRIs closest to death. Autopsy CAA burden was quantified in each region including leptomeningeal/cortical and capillary CAA. By a clustering approach, we examined the relationship among CAA variables and performed principal component analysis (PCA) for dimension reduction to produce two scores from these 15 interrelated predictors. Hurdle models assessed relationships between principal components and lobar CMBs.

resultsMRI-based CMBs appeared in 20/54 (37%). 10 participants had ≥2 lobar-only CMBs. The first two components of the PCA analysis of the CAA variables explained 74% variability. The first rotated component (RPC1) consisted of leptomeningeal and cortical CAA and the second rotated component of capillary CAA (RPC2). Both the leptomeningeal and cortical component and the capillary component correlated with lobar-only CMBs. The capillary CAA component outperformed the leptomeningeal and cortical CAA component in predicting lobar CMBs. Both capillary and the leptomeningeal/cortical components correlated with number of lobar CMBs.

conclusionCapillary and leptomeningeal/cortical scores correlated with lobar CMBs on MRI but lobar CMBs were more closely associated with the capillary component. The capillary component correlated with APOEɛ4, highlighting lobar CMBs as one aspect of CAA phenotypic diversity. More CMBs also increase the probability of underlying CAA.

Indexed as

PhenotypeAgedAged, 80 and overBrainCerebral Amyloid AngiopathyCerebral HemorrhageFemaleHumansMagnetic Resonance ImagingMaleMiddle AgedAlzheimer’s diseasecapillariescerebral amyloid angiopathyneuropathology

Identifiers

PMID33720897
PMCPMC8113155
OpenAlexW3136676529

What OpenQuestion holds

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Registered trials

None linked

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.