Evidence map›Paper›PMID 30062722›Full record

ArticleBrain pathology (Zurich, Switzerland)2018

The association between hypertensive arteriopathy and cerebral amyloid angiopathy in spontaneously hypertensive stroke-prone rats.

Solveig Jandke, Cornelia Garz, Daniel Schwanke, Michael Sendtner, Hans-Jochen Heinze, Roxana O Carare, Stefanie Schreiber

Open access · hybridAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
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  4. Typical distribution of hypertensive cerebral microbleed: a matched case-control study using primary aldosteronism.Hypertension research : official journal of the Japanese Society of Hypertension · 2025
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  18. Brain amyloid and vascular risk are related to distinct white matter hyperintensity patterns.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  19. Article
  20. Review
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 4 institutions in 2 countries.

Solveig JandkeDepartment of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
Cornelia GarzDepartment of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
Daniel SchwankeDepartment of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
Michael SendtnerInstitute of Clinical Neurobiology, University of Würzburg, Germany.
Hans-Jochen HeinzeDepartment of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
Roxana O CarareFaculty of Medicine, University of Southampton, UK.
Stefanie SchreiberDepartment of Neurology, Otto-von-Guericke University, Magdeburg, Germany.
Otto-von-Guericke University Magdeburg · DEGerman Center for Neurodegenerative Diseases · DEUniversity of Southampton · GBUniversity of Würzburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We aimed to test the hypothesis that in spontaneously hypertensive stroke-prone rats (SHRSP), non-amyloid cerebral small vessel disease/hypertensive arteriopathy (HA) results in vessel wall injury that may promote cerebral amyloid angiopathy (CAA). Our study comprised 21 male SHRSP (age 17-44 weeks) and 10 age- and sex-matched Wistar control rats, that underwent two-photon (2PM) imaging of the arterioles in the parietal cortex using Methoxy-X04, Dextran and cerebral blood flow (CBF) measurements. Our data suggest that HA in SHRSP progresses in a temporal and age-dependent manner, starting from small vessel wall damage (stage 1A), proceeding to CBF reduction (stage 1B), non-occlusive (stage 2), and finally, occlusive thrombi (stage 3). Wistar animals also demonstrated small vessel wall damage, but were free of any of the later HA stages. Nearly half of all SHRSP additionally displayed vascular Methoxy-X04 positivity indicative of cortical CAA. Vascular β-amyloid deposits were found in small vessels characterized by thrombotic occlusions (stage 2 or 3). Post-mortem analysis of the rat brains confirmed the findings derived from intravital 2PM microscopy. Our data thus overall suggest that advanced HA may play a role in CAA development with the two small vessel disease entities might be related to the same pathological spectrum of the aging brain.

Indexed as

AgingAmyloid beta-PeptidesAnimalsArteriolesAutopsyBrainCerebral Amyloid AngiopathyCerebral Small Vessel DiseasesCerebrovascular CirculationDisease Models, AnimalFemaleHypertensionIntravital MicroscopyMaleRatsRats, Inbred SHRAmyloid beta-Peptidescerebral amyloid angiopathycerebral small vessel diseasehypertensive arteriopathyintravital imagingspontaneously hypertensive stroke-prone rat

Identifiers

PMID30062722
PMCPMC8028507
OpenAlexW2887695564

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.