Evidence map›Paper›PMID 30990880›Full record

ArticleJournal of neuropathology and experimental neurology2019

Peri-Infarct Upregulation of the Oxytocin Receptor in Vascular Dementia.

Erin C McKay, John S Beck, Sok Kean Khoo, Karl J Dykema, Sandra L Cottingham, Mary E Winn, Henry L Paulson, Andrew P Lieberman, Scott E Counts

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuropathology and experimental neurology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
12.1field-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

83 citing papers in PubMed, 112 citations in OpenAlex.

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23 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

9 authors at 6 institutions in 1 country.

Erin C McKayDepartment of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, Michigan.
John S BeckDepartment of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, Michigan.
Sok Kean KhooDepartment of Cell and Molecular Biology, Grand Valley State University, Grand Rapids, Michigan.
Karl J DykemaBioinformatics and Biostatistics Core, Van Andel Research Institute, Grand Rapids, Michigan.
Sandra L CottinghamDepartment of Pathology, Spectrum Health and Helen DeVos Children's Hospital, Grand Rapids, Michigan.
Mary E WinnBioinformatics and Biostatistics Core, Van Andel Research Institute, Grand Rapids, Michigan.
Henry L PaulsonDepartment of Neurology, University of Michigan, Ann Arbor, Michigan.
Andrew P LiebermanDepartment of Pathology, University of Michigan, Ann Arbor, Michigan.
Scott E CountsDepartment of Translational Science and Molecular Medicine, Michigan State University, Grand Rapids, Michigan.
Michigan State University · USUniversity of Michigan–Ann Arbor · USVan Andel Institute · USGrand Valley State University · USHelen DeVos Children's Hospital · USMercy Health Saint Mary's · US

Funding

TAU, AB, SYNUCLEIN AND NITRATIVE/OXIDATIVE DAMAGE IN MCIP01AG014449 · NIA · UNIVERSITY OF PITTSBURGH · PI COUNTS, SCOTT E · 1997 to 2024
$39.7M
Michigan Alzheimer's Disease Core CenterP30AG053760 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALBIN, ROGER L · 2016 to 2020
$10.1M
Molecular profiling of familial and sporadic Alzheimer's diseaseR21AG053581 · NIA · MICHIGAN STATE UNIVERSITY · PI COUNTS, SCOTT E · 2016 to 2017
$426k
NIA NIH HHS P01 AG014449NIA NIH HHS P30 AG053760NIA NIH HHS R21 AG053581
6 · The paper itself

Abstract

Vascular dementia (VaD) is cognitive decline linked to reduced cerebral blood perfusion, yet there are few therapeutic options to protect cognitive function following cerebrovascular accidents. The purpose of this study was to profile gene expression changes unique to VaD to identify and characterize disease relevant changes that could offer clues for future therapeutic direction. Microarray-based profiling and validation studies of postmortem frontal cortex samples from VaD, Alzheimer disease, and age-matched control subjects revealed that the oxytocin receptor (OXTR) was strongly and differentially upregulated in VaD. Further characterization in fixed tissue from the same cases showed that OXTR upregulation occurs de novo around and within microinfarcts in peri-infarct reactive astrocytes as well as within vascular profiles, likely on microvascular endothelial cells. These results indicate that increased OXTR expression in peri-infarct regions may be a specific response to microvascular insults. Given the established OXTR signaling cascades that elicit antioxidant, anti-inflammatory, and pro-angiogenic responses, the present findings suggest that de novo OXTR expression in the peri-infarct space is a tissue-protective response by astroglial and vascular cells in the wake of ischemic damage that could be exploited as a therapeutic option for the preservation of cognition following cerebrovascular insults.

Indexed as

AgedAged, 80 and overCerebral InfarctionDementia, VascularFemaleFrontal LobeGene Regulatory NetworksHumansMaleMiddle AgedReceptors, OxytocinUp-RegulationReceptors, OxytocinAlzheimer diseaseAstrocvytesMicroinfarctsMicrovascular endothelial cellsOxytocin receptorVascular dementia

Identifiers

PMID30990880
PMCPMC6467199
OpenAlexW2937258271

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.