Evidence map›Paper›PMID 31522299›Full record

ArticleCellular and molecular neurobiology2020

Role of Delayed Neuroglial Activation in Impaired Cerebral Blood Flow Restoration Following Comorbid Injury.

Zareen Amtul, Jasmine Randhawa, Abdullah N Najdat, David J Hill, Edith J Arany

Erratum issuedOpen access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 38% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Zareen AmtulDepartment of Anatomy and Cell Biology, University of Western Ontario, London, N6A 5C1, Canada. zareen.amtul@gmail.com.
Jasmine RandhawaDepartment of Biology, University of Western Ontario, London, N6A 5B7, Canada.
Abdullah N NajdatDepartment of Biology, University of Western Ontario, London, N6A 5B7, Canada.
David J HillDepartments of Medicine, Physiology, and Pharmacology, and Pediatrics, University of Western Ontario, London, N6A 5C1, Canada.
Edith J AranyDepartment of Pathology and Laboratory Medicine, University of Western Ontario, London, N6A 5C1, Canada.
Western University · CALawson Health Research Institute · CA

Funding

CIHR R1478A47
6 · The paper itself

Abstract

Besides other causes, ischemia and Alzheimer's disease pathology is also linked to decreased cerebral blood flow (CBF). There is little or no consensus about the role of neuroglial cells in maintaining CBF in various neuropathologies. This consensus becomes scarcer when it comes to clinical and experimental cases of comorbid Abeta-amyloid (Aβ) toxicity and ischemia. Here, a comorbid rat model of Aβ toxicity and endothelin-1 induced ischemia (ET1) not only demonstrated the appearance of axotomized phagocytosed pyknotic neurons (NeuN) immediately after the injury, but also showed a diversity of continuously changing neuroglia (MHC Class II/OX6, Iba1) and macrophage (Iba1/CD68) phenotypes with round, stout somas, and retracted processes. This is indicative of a response to a concomitant increase in large fluid-filled spaces due to the vascular leakage. Ironically 4 weeks after the injury despite a conclusive reduction in neurons, CBF restoration in ET1 rats was associated with a massive increase in neuroglial cell numbers, hypertrophy, ramification, and soma sizes bordering the continuously reducing lesion core and inflamed vasculature, possibly to shield their leaky phenotype. Astrocytes were also found to be releasing matrix metalloproteinase9 (MMP9), which stabilized matrix ligand β-dystroglycan (β-DG) in repaired or functional vessels. Changing neuroglia phenotypes, responses, motility, astrocytic recruitment of MMP9, and β-DG stabilization implies the role of communication between neuroglia and endothelium in recovering CBF, in the absence of neurons, in ET1 rats compared to Aβ+ET1 rats, which showed characteristics delayed neuroglial activation. Stimulation of timely neuroglial reactivity may serve as a viable strategy to compensate for the neuronal loss in restoring CBF in comorbid cases of ischemia and Aβ toxicity.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesBrainBrain IschemiaCerebrovascular CirculationDisease Models, AnimalMaleNeurogliaNeuronsRatsRats, WistarReperfusion InjuryAmyloid beta-PeptidesAstrocytesCerebral blood flowIschemiaMicrogliaNeurovascular unitβ-Amyloid

Identifiers

PMID31522299
PMCPMC11448772
OpenAlexW2972446148

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.