Evidence map›Paper›PMID 31776837›Full record

ReviewTranslational stroke research2020

From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation.

Romain Goulay, Luis Mena Romo, Elly M Hol, Rick M Dijkhuizen

Open access · hybridAbstract readReview
In one paragraph

Review in Translational stroke research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 92 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
92citing papers in PubMed, 3 pooled it
9.7field-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

92 citing papers in PubMed, 3 syntheses or guidelines pooled it, 134 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Article
  6. Blood-Based Biomarkers for Post-Stroke Cognitive Impairment.Current issues in molecular biology · 2026
    Review
  7. Article
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  16. Observational
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32 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 2 countries.

Romain GoulayBiomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht University, Yalelaan 2, 3584 CM, Utrecht, The Netherlands. romain.goulay@def.gouv.fr.
Luis Mena RomoDepartment of Neurology, University Hospital Sant Juan Despi Moises Broggi, Barcelona, Spain.
Elly M HolDepartment of Translational Neuroscience, UMC Utrecht Brain Center, University Medical Center Utrecht, Utrecht University, Utrecht, The Netherlands.
Rick M DijkhuizenBiomedical MR Imaging and Spectroscopy Group, Center for Image Sciences, University Medical Center Utrecht, Utrecht University, Yalelaan 2, 3584 CM, Utrecht, The Netherlands. r.m.dijkhuizen@umcutrecht.nl.ORCID http://orcid.org/0000-0002-4623-4078
Utrecht University · NLHospital de Sant Joan Despí Moisès Broggi · ESRoyal Netherlands Academy of Arts and Sciences · NL

Funding

EU Joint Programme - Neurodegenerative Disease Research through ZonMW (NL) 733051067
6 · The paper itself

Abstract

Stroke and Alzheimer's disease (AD) are cerebral pathologies with high socioeconomic impact that can occur together and mutually interact. Vascular factors predisposing to cerebrovascular disease have also been specifically associated with development of AD, and acute stroke is known to increase the risk to develop dementia.Despite the apparent association, it remains unknown how acute cerebrovascular disease and development of AD are precisely linked and act on each other. It has been suggested that this interaction is strongly related to vascular deposition of amyloid-β (Aβ), i.e., cerebral amyloid angiopathy (CAA). Furthermore, the blood-brain barrier (BBB), perivascular space, and the glymphatic system, the latter proposedly responsible for the drainage of solutes from the brain parenchyma, may represent key pathophysiological pathways linking stroke, Aβ deposition, and dementia.In this review, we propose a hypothetic connection between CAA, stroke, perivascular space integrity, and dementia. Based on relevant pre-clinical research and a few clinical case reports, we speculate that impaired perivascular space integrity, inflammation, hypoxia, and BBB breakdown after stroke can lead to accelerated deposition of Aβ within brain parenchyma and cerebral vessel walls or exacerbation of CAA. The deposition of Aβ in the parenchyma would then be the initiating event leading to synaptic dysfunction, inducing cognitive decline and dementia. Maintaining the clearance of Aβ after stroke could offer a new therapeutic approach to prevent post-stroke cognitive impairment and development into dementia.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBlood-Brain BarrierCerebral Amyloid AngiopathyDementiaGlymphatic SystemHumansProtein Aggregation, PathologicalStrokeAmyloid beta-PeptidesAlzheimer’s diseaseBeta-amyloidCerebral amyloid angiopathyDementiaStroke

Identifiers

PMID31776837
PMCPMC7340665
OpenAlexW2990679316

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.