Evidence map›Paper›PMID 24725245›Full record

ArticleBrain pathology (Zurich, Switzerland)2015

Comorbid rat model of ischemia and β-amyloid toxicity: striatal and cortical degeneration.

Zareen Amtul, Shawn N Whitehead, Robin J Keeley, John Bechberger, Alicia L Fisher, Robert J McDonald, Christian C Naus, David G Munoz, David F Cechetto

Open access · greenAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 36 citations in OpenAlex.

  1. Rodent Models of Post-Stroke Dementia.International journal of molecular sciences · 2022
    Review
  2. Article
  3. Article
  4. Review
  5. Preventing dementia by preventing stroke: The Berlin Manifesto.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2019
    Review
  6. Article
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  10. A Single-Nucleotide Polymorphism in 3'-Untranslated Region of Endothelin-1 Reduces Risk of Dementia After Ischemic Stroke.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  11. Selective astrocytic endothelin-1 overexpression contributes to dementia associated with ischemic stroke by exaggerating astrocyte-derived amyloid secretion.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Article
  12. Article
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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

9 authors at 4 institutions in 1 country.

Zareen AmtulCIHR Group on Vascular Cognitive Impairment, Department of Anatomy and Cell Biology, Western University, London, ON, Canada.
Shawn N Whitehead
Robin J Keeley
John Bechberger
Alicia L Fisher
Robert J McDonald
Christian C Naus
David G Munoz
David F Cechetto
University of Lethbridge · CAWestern University · CAUniversity of British Columbia · CAUniversity of Toronto · CA

Funding

Canadian Institutes of Health Research R1478A47
6 · The paper itself

Abstract

Levels of cerebral amyloid, presumably β-amyloid (Abeta), toxicity and the incidence of cortical and subcortical ischemia increases with age. However, little is known about the severe pathological condition and dementia that occur as a result of the comorbid occurrence of this vascular risk factor and Abeta toxicity. Clinical studies have indicated that small ischemic lesions in the striatum are particularly important in generating dementia in combination with minor amyloid lesions. These cognitive deficits are highly likely to be caused by changes in the cortex. In this study, we examined the viability and morphological changes in microglial and neuronal cells, gap junction proteins (connexin43) and neuritic/axonal retraction (Fer Kinase) in the striatum and cerebral cortex using a comorbid rat model of striatal injections of endothelin-1 (ET1) and Abeta toxicity. The results demonstrated ventricular enlargement, striatal atrophy, substantial increases in β-amyloid, ramified microglia and increases in neuritic retraction in the combined models of stroke and Abeta toxicity. Changes in connexin43 occurred equally in both groups of Abeta-treated rats, with and without focal ischemia. Although previous behavioral tests demonstrated impairment in memory and learning, the visual discrimination radial maze task did not show significant difference, suggesting the cognitive impairment in these models is not related to damage to the dorsolateral striatum. These results suggest an insight into the relationship between cortical/striatal atrophy, pathology and functional impairment.

Indexed as

Amyloid beta-PeptidesAmyloidosisAnimalsBrain IschemiaCerebral CortexComorbidityConnexin 43Corpus StriatumDisease Models, AnimalEndothelin-1MaleMaze LearningMicrogliaNerve DegenerationNeuritesNeuronsAmyloid beta-PeptidesConnexin 43Endothelin-1Protein-Tyrosine Kinasesproto-oncogene protein c-fes-fpsaxonal retractionbeta-amyloidcellular degenerationinfarctmicrogliosis

Identifiers

PMID24725245
PMCPMC8029334
OpenAlexW1520606530

What Socratic holds

Textmetadata
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 Socratic graph.