Evidence map›Paper›PMID 40895091›Full record

ArticleNeuroglia (Basel, Switzerland)2024

Dynamic Neuro-Glial-Vascular Responses in a Mouse Model of Vascular Cognitive Impairment.

Ki Jung Kim, Rachel E Patterson, Juan Ramiro Diaz, Philip O'Herron, Weston Bush, Ferdinand Althammer, Javier E Stern, Michael W Brands, Zsolt Bagi, Jessica A Filosa

Abstract read
In one paragraph

Article in Neuroglia (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
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

10 authors.

Ki Jung KimDepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.ORCID 0009-0008-6901-3463
Rachel E PattersonDepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.ORCID 0009-0009-4734-8761
Juan Ramiro DiazDepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.ORCID 0009-0007-4925-6049
Philip O'HerronDepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.ORCID 0000-0002-8137-9432
Weston BushDepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
Ferdinand AlthammerNeuroscience Institute, Georgia State University, Atlanta, GA 30302, USA.
Javier E SternNeuroscience Institute, Georgia State University, Atlanta, GA 30302, USA.
Michael W BrandsDepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
Zsolt BagiDepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.
Jessica A FilosaDepartment of Physiology, Medical College of Georgia, Augusta University, Augusta, GA 30912, USA.ORCID 0000-0001-7536-2039

Funding

Uncovering the physiological role of functional hyperemiaR01NS126920 · NINDS · AUGUSTA UNIVERSITY · PI Philip O'Herron · 2023 to 2026
$1.8M
Clinically unscreened vasculo-glial-neuronal coupling is critical for physiological brain functionR01NS097818 · NINDS · AUGUSTA UNIVERSITY · PI FILOSA, JESSICA A · 2017 to 2021
$1.8M
NINDS NIH HHS R01 NS097818NINDS NIH HHS R01 NS126920
6 · The paper itself

Abstract

Background: Chronic hypoperfusion is a risk factor for neurodegenerative diseases. However, the sequence of events driving ischemia-induced functional changes in a cell-specific manner is unclear. Methods: To address this gap in knowledge, we used the bilateral common carotid artery stenosis (BCAS) mouse model, and evaluated progressive functional changes to neurons, arterioles, astrocytes, and microglial cells at 14 and 28 days post-BCAS surgery. To assess the neuro-glio-vascular response to an acute ischemic insult, brain slices were superfused with low O Results: Our data showed no changes to the basic membrane properties of cortical pyramidal neurons. On the other hand, astrocyte activity was characterized by a progressive increase in the resting Ca Conclusions: Together, these data suggest that, in young mice, BCAS leads to vascular dysfunction (e.g., impaired vasodilation in parenchymal arterioles), and in the absence of neuronal dysfunction, mild ischemia is associated with the activation of glial-derived neuroprotective signals.

Indexed as

adenosineastrocytecalciumhypoperfusionneurovascular unit

Identifiers

PMID40895091
PMCPMC12393155

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Registered trials

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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.