Evidence map›Paper›PMID 30519973›Full record

ArticleAngiogenesis2019

Mouse models of Alzheimer's disease cause rarefaction of pial collaterals and increased severity of ischemic stroke.

Hua Zhang, Bo Jin, James E Faber

Open access · hybridAbstract read
In one paragraph

Article in Angiogenesis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

31 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
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  11. Vascular Biology.Stroke · 2021
    Review
  12. Article
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  14. Hypoxia induces de novo formation of cerebral collaterals and lessens the severity of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    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

3 authors at 2 institutions in 2 countries.

Hua ZhangDepartment of Cell Biology and Physiology, University of North Carolina at Chapel Hill, 6309 MBRB, Chapel Hill, NC, 27599-7545, USA.
Bo JinZhejiang Chinese Medical University, Hangzhou, China.
James E FaberDepartment of Cell Biology and Physiology, University of North Carolina at Chapel Hill, 6309 MBRB, Chapel Hill, NC, 27599-7545, USA. jefaber@med.unc.edu.
University of North Carolina at Chapel Hill · USZhejiang Chinese Medical University · CN

Funding

Targeting the Pial Collateral Circulation for Mitigation of Cerebral IschemiaR01NS083633 · NINDS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZHANG, HUA · 2013 to 2023
$4.5M
NINDS NIH HHS NS083633
6 · The paper itself

Abstract

Vascular dysfunction contributes to the progression and severity of Alzheimer's disease (AD). Patients with AD also sustain larger infarctions after ischemic stroke; however, the responsible mechanisms are unknown. Pial collaterals are the primary source of protection in stroke. Unfortunately, natural aging and other vascular risk factors cause a decline in collateral number and diameter (rarefaction) and an increase in stroke severity. Herein, we tested the hypothesis that AD accelerates age-induced collateral rarefaction and examined potential underlying mechanisms. Triple and double transgenic mouse models of AD both sustained collateral rarefaction by 8 months of age, well before the onset of rarefaction caused by aging alone (16 months of age). Rarefaction, which did not progress further at 18 months of age, was accompanied by a twofold increase in infarct volume after MCA occlusion. AD did not induce rarefaction of similarly sized pial arterioles or penetrating arterioles. Rarefaction was minimal and occurred only at 18 months of age in a parenchymal vascular amyloid-beta model of AD. Rarefaction was not associated with amyloid-beta deposition on collaterals or pial arteries, nor was plaque burden or CD11b

Indexed as

Disease Models, AnimalAgingAlzheimer DiseaseAmyloid beta-Protein PrecursorAnimalsArteriolesBrain IschemiaCell CountCerebral VeinsCerebrovascular CirculationCollateral CirculationHumansMiceMice, TransgenicNeovascularization, PhysiologicPresenilin-1Amyloid beta-Protein PrecursorMapt protein, mousePresenilin-1presenilin 1, mousetau ProteinsAlzheimer’s diseaseCerebral amyloid angiopathyCollateral circulationStroke

Identifiers

PMID30519973
PMCPMC6475514
OpenAlexW2903218349

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.