Evidence map›Paper›PMID 25716356›Full record

ArticleNeurology2015

Cerebral amyloid angiopathy with and without hemorrhage: evidence for different disease phenotypes.

Andreas Charidimou, Sergi Martinez-Ramirez, Ashkan Shoamanesh, Jamary Oliveira-Filho, Matthew Frosch, Anastasia Vashkevich, Alison Ayres, Jonathan Rosand, Mahmut Edip Gurol, Steven M Greenberg and 1 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 3 pooled it
10.7field-weighted citation impact, top 1% 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

72 citing papers in PubMed, 3 syntheses or guidelines pooled it, 118 citations in OpenAlex.

  1. Neurology · 2019
    Pooled it
  2. Pooled it
  3. Pooled it
  4. Factors associated with intracerebral hemorrhage in confirmed cerebral amyloid angiopathy.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  5. Article
  6. Article
  7. Amyloid-Related Imaging Abnormality (ARIA) Beyond the APOE-ε4 Allele.Chronic diseases and translational medicine · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Sex differences in histopathological markers of cerebral amyloid angiopathy and related hemorrhage.International journal of stroke : official journal of the International Stroke Society · 2024
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Andreas CharidimouFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston. acharidimou@mgh.harvard.edu.
Sergi Martinez-RamirezFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Ashkan ShoamaneshFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Jamary Oliveira-FilhoFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Matthew FroschFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Anastasia VashkevichFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Alison AyresFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Jonathan RosandFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Mahmut Edip GurolFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Steven M GreenbergFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
Anand ViswanathanFrom the Department of Brain Repair and Rehabilitation (A.C.), UCL Institute of Neurology and The National Hospital for Neurology and Neurosurgery, London, UK; and the Hemorrhagic Stroke Research Program, Stroke Research Center, Department of Neurology (A.C., S.M.-R., A.S., J.O.-F., A. Vashkevich, A.A., J.R., M.E.G., S.M.G., A. Viswanathan), C.S. Kubik Laboratory for Neuropathology (M.F.), Division of Neurocritical Care and Emergency Neurology (J.R.), and Center for Human Genetic Research (J.R.), Massachusetts General Hospital, Harvard Medical School, Boston.
University College London · GBNational Hospital for Neurology and Neurosurgery · GB

Funding

THE ROLE OF ADVANCED CAA IN ALZHEIMER'S DEMENTIAP50AG005134 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI HYMAN, BRADLEY T. · 1985 to 2018
$42.1M
Research Education ComponentP30AG062421 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI Alberto Serrano-Pozo · 2019 to 2026
$36.5M
Specialized Programs of Translational Research in Acute Stroke at the PartnersP50NS051343 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GREENBERG, STEVEN M · 2006 to 2013
$17.5M
Vascular Pathology in Early and Asymptomatic Cerebral Amyloid AngiopathyR01AG047975 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI VISWANATHAN, ANAND · 2014 to 2025
$7.5M
Molecular Neuroimaging of Disease Mechanisms in Cerebral Amyloid AngiopathyK23NS083711 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI GUROL, MAHMUT EDIP · 2014 to 2018
$988k
Effect of White Matter Disease on Gait and Balance in Cerebral Amyloid AngiopathyK23AG028726 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI VISWANATHAN, ANAND · 2010 to 2014
$823k
NIA NIH HHS K23 AG028726NIA NIH HHS P30 AG062421NIA NIH HHS P50 AG005134NIA NIH HHS R01 AG047975NINDS NIH HHS K23 NS083711NINDS NIH HHS P50 NS051343
6 · The paper itself

Abstract

objectiveTo gain insight into different cerebral amyloid angiopathy (CAA) phenotypes and mechanisms, we investigated cortical superficial siderosis (CSS), a new imaging marker of the disease, and its relation with APOE genotype in patients with pathologically proven CAA, who presented with and without intracerebral hemorrhage (ICH).

methodsMRI scans of 105 patients with CAA pathologic confirmation and MRI were analyzed for CSS (focal, ≤3 sulci; disseminates, ≥4 sulci) and other imaging markers. We compared pathologic, imaging, and APOE genotype data between subjects with vs without ICH, and investigated associations between CSS and APOE genotype.

resultsOur cohort consisted of 54 patients with CAA with symptomatic lobar ICH and 51 without ICH. APOE genotype was available in 53 patients. More than 90% of pathology samples in both groups had neuritic plaques, whereas neurofibrillary tangles were more commonly present in the patients without ICH (87% vs 42%, p < 0.0001). There was a trend for patients with CAA with ICH to more commonly have APOE ε2 (48.7% vs 21.4%, p = 0.075), whereas patients without ICH were more likely to be APOE ε4 carriers (85.7% vs 53.9%, p = 0.035). Disseminated CSS was considerably commoner in patients with ICH (33.3% vs 5.9%, p < 0.0001). In logistic regression, disseminated CSS was associated with APOE ε2 (but not APOE ε4) (odds ratio 5.83; 95% confidence interval 1.49-22.82, p = 0.011).

conclusionsThis neuropathologically defined CAA cohort suggests that CSS and APOE ε2 are related to the hemorrhagic expression of the disease; APOE ε4 is enriched in nonhemorrhagic CAA. Our study emphasizes the concept of different CAA phenotypes, suggesting divergent pathophysiologic mechanisms.

Indexed as

Cerebral Amyloid AngiopathyCerebral HemorrhageHemosiderosisAgedApolipoprotein E2Apolipoprotein E4BiomarkersCerebral CortexFemaleGenotypeHumansMagnetic Resonance ImagingMalePhenotypeApolipoprotein E2Apolipoprotein E4Biomarkers

Identifiers

PMID25716356
PMCPMC4366086
OpenAlexW2046459425

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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.