Evidence map›Paper›PMID 25790832›Full record

ArticleJournal of Alzheimer's disease : JAD2015

Inflammation Combined with Ischemia Produces Myelin Injury and Plaque-Like Aggregates of Myelin, Amyloid-β and AβPP in Adult Rat Brain.

Xinhua Zhan, Christopher Cox, Bradley P Ander, Dazhi Liu, Boryana Stamova, Lee-Way Jin, Glen C Jickling, Frank R Sharp

Open access · bronzeAbstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2015. 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
2.6field-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, 42 citations in OpenAlex.

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  5. The role of serum/glucocorticoid-regulated kinase 1 in brain function following cerebral ischemia.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
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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

8 authors at 2 institutions in 1 country.

Xinhua ZhanDepartment of Neurology, MIND Institute, University of California at Davis, Sacramento, CA, USA.
Christopher CoxDepartment of Neurology, MIND Institute, University of California at Davis, Sacramento, CA, USA.
Bradley P AnderDepartment of Neurology, MIND Institute, University of California at Davis, Sacramento, CA, USA.
Dazhi LiuDepartment of Neurology, MIND Institute, University of California at Davis, Sacramento, CA, USA.
Boryana StamovaDepartment of Neurology, MIND Institute, University of California at Davis, Sacramento, CA, USA.
Lee-Way JinAlzheimer's Disease Center, University of California at Davis, Sacramento, CA, USA.
Glen C JicklingDepartment of Neurology, MIND Institute, University of California at Davis, Sacramento, CA, USA.
Frank R SharpDepartment of Neurology, MIND Institute, University of California at Davis, Sacramento, CA, USA.
University of California, Davis · USAlzheimer’s Disease Neuroimaging Initiative · US

Funding

UC Davis Alzheimer's Disease Core CenterP30AG010129 · NIA · UNIVERSITY OF CALIFORNIA DAVIS · PI DECARLI, CHARLES · 1991 to 2020
$28.3M
NIA NIH HHS P30 AG010129NIA NIH HHS P30AG10129-21
6 · The paper itself

Abstract

backgroundIschemia, white matter injury, and Alzheimer's disease (AD) pathologies often co-exist in aging brain. How one condition predisposes to, interacts with, or perhaps causes the others remains unclear.

objectivesTo better understand the link between ischemia, white matter injury, and AD, adult rats were administered lipopolysaccharide (LPS) to serve as an inflammatory stimulus, and 24 h later subjected to 20-min focal cerebral ischemia (IS) followed by 30-min hypoxia (H).

methodsMyelin and axonal damage, as well as amyloid-β (Aβ) and amyloid-β protein precursor (AβPP) deposition were examined by Western blot and immunocytochemistry following LPS/IS/H. Findings were compared to the 5XFAD mouse AD brain.

resultsMyelin/axonal injury was observed bilaterally in cortex following LPS/IS/H, along with an increase in IL-1, granzyme B, and LPS. AβPP deposition was present in ischemic striatum in regions of myelin loss. Aβ(1-42) and AβPP were deposited in small foci in ischemic cortex that co-localized with myelin aggregates. In the 5XFAD mouse AD model, cortical amyloid plaques also co-localized with myelin aggregates.

conclusionsLPS/IS/H produce myelin injury and plaque-like aggregates of myelin. AβPP and Aβ co-localize with these myelin aggregates.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainBrain IschemiaDisease Models, AnimalInflammationLipopolysaccharidesMaleMiceMice, TransgenicMyelin Basic ProteinMyelin SheathPeptide FragmentsPlaque, AmyloidAmyloid beta-Peptidesamyloid beta-protein (1-42)Amyloid beta-Protein PrecursorLipopolysaccharidesMyelin Basic ProteinPeptide FragmentsAlzheimer’s diseaseamyloid plaquesamyloid-βamyloid-β protein precursorhypoxialipopolysaccharidemyelinmyelin basic protein

Identifiers

PMID25790832
PMCPMC4878315
OpenAlexW1692550889

What OpenQuestion 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 OpenQuestion graph.