Evidence map›Paper›PMID 25519173›Full record

ArticleActa neuropathologica communications2014

Spontaneous white matter damage, cognitive decline and neuroinflammation in middle-aged hypertensive rats: an animal model of early-stage cerebral small vessel disease.

Daniel Kaiser, Gesa Weise, Karoline Möller, Johanna Scheibe, Claudia Pösel, Sebastian Baasch, Matthias Gawlitza, Donald Lobsien, Kai Diederich, Jens Minnerup and 3 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 2 pooled it
6.8field-weighted citation impact, top 3% 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

112 citing papers in PubMed, 2 syntheses or guidelines pooled it, 213 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. The role of inflammation in cerebral small vessel disease and vascular cognitive impairment, and therapeutic implications.International journal of stroke : official journal of the International Stroke Society · 2026
    Review
  6. Article
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  8. Cytoprotection Concepts for Ischemic Stroke in the Recanalization Era.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  9. Current updates on latest basic research of scientific relevance in hypertensive dementia.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
    Review
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52 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

13 authors at 4 institutions in 1 country.

Daniel KaiserFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. daniel.kaiser@izi.fraunhofer.de.
Gesa WeiseFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. gesa.weise@izi.fraunhofer.de.
Karoline MöllerFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. karoline.moeller@izi.fraunhofer.de.
Johanna ScheibeFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. johanna.scheibe@izi.fraunhofer.de.
Claudia PöselFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. claudia.poesel@izi.fraunhofer.de.
Sebastian BaaschFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. sebastian.baasch@izi.fraunhofer.de.
Matthias GawlitzaDepartment of Radiology, University of Leipzig, Leipzig, Germany. Matthias.Gawlitza@medizin.uni-leipzig.de.
Donald LobsienDepartment of Neuroradiology, University of Leipzig, Leipzig, Germany. donald.lobsien@medizin.uni-leipzig.de.
Kai DiederichDepartment of Neurology, University of Münster, Münster, Germany. kai.diederich@uni-muenster.de.
Jens MinnerupDepartment of Neurology, University of Münster, Münster, Germany. minnerup@uni-muenster.de.
Alexander KranzFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. alexander.kranz@izi.fraunhofer.de.
Johannes BoltzeFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. johannes.boltze@izi.fraunhofer.de.
Daniel-Christoph WagnerFraunhofer Institute for Cell Therapy and Immunology, Perlickstraße 1, 04103, Leipzig, Germany. daniel-christoph.wagner@izi.fraunhofer.de.
Fraunhofer Institute for Cell Therapy and Immunology · DELeipzig University · DEUniversity Hospital Münster · DEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionCerebral small vessel disease (cSVD) is one of the most prevalent neurological disorders. The progressive remodeling of brain microvessels due to arterial hypertension or other vascular risk factors causes subtle, but constant cognitive decline through to manifest dementia and substantially increases the risk for stroke. Preliminary evidence suggests the contribution of the immune system to disease initiation and progression, but a more detailed understanding is impaired by the unavailability of appropriate animal models. Here, we introduce the spontaneously hypertensive rat (SHR) as a model for early onset cSVD and unveiled substantial immune changes in conjunction with brain abnormalities that resemble clinical findings.

resultsIn contrast to age-matched normotensive Wistar Kyoto (WKY) rats, male SHR exhibited non-spatial memory deficits. Magnetic resonance imaging showed brain atrophy and a reduction of white matter volumes in SHR. Histological analyses confirmed white matter demyelination and unveiled a circumscribed blood brain barrier dysfunction in conjunction with micro- and macrogliosis in deep cortical regions. Flow cytometry and histological analyses further revealed substantial disparities in cerebral CD45high leukocyte counts and distribution patterns between SHR and WKY. SHR showed lower counts of T cells in the choroid plexus and meningeal spaces as well as decreased interleukin-10 levels in the cerebrospinal fluid. On the other hand, both T and NK cells were significantly augmented in the SHR brain microvasculature.

conclusionsOur results indicate that SHR share behavioral and neuropathological characteristics with human cSVD patients and further undergird the relevance of immune responses for the initiation and progression of cSVD.

Indexed as

Disease Models, AnimalAnimalsAtrophyBlood-Brain BarrierBrainCerebral Small Vessel DiseasesCognition DisordersGliosisInterleukin-10Killer Cells, NaturalLeukocyte Common AntigensLeukocytesMaleMemory DisordersNeuroimmunomodulationOrgan SizeInterleukin-10Leukocyte Common AntigensPtprc protein, rat

Identifiers

PMID25519173
PMCPMC4279586
OpenAlexW2168558768

What OpenQuestion holds

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LicenceCC BY
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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.