Evidence map›Paper›PMID 29445328›Full record

ArticleFrontiers in cellular neuroscience2018

Hippocampal Atrophy Following Subarachnoid Hemorrhage Correlates with Disruption of Astrocyte Morphology and Capillary Coverage by AQP4.

Maryam Anzabi, Maryam Ardalan, Nina K Iversen, Ali H Rafati, Brian Hansen, Leif Østergaard

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.2field-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

34 citing papers in PubMed, 44 citations in OpenAlex.

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  12. Pathophysiology, Management, and Therapeutics in Subarachnoid Hemorrhage and Delayed Cerebral Ischemia: An Overview.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
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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

6 authors at 1 institution in 2 countries.

Maryam AnzabiDepartment of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark.
Maryam ArdalanDepartment of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark.
Nina K IversenDepartment of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark.
Ali H RafatiTranslational Neuropsychiatry Unit, Department of Clinical Medicine, Aarhus University, Risskov, Denmark.
Brian HansenDepartment of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark.
Leif ØstergaardDepartment of Clinical Medicine, Center of Functionally Integrative Neuroscience and MINDLab, Aarhus University, Aarhus, Denmark.
Aarhus University · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite successful management of ruptured intracranial aneurysm following subarachnoid hemorrhage (SAH), delayed cerebral ischemia (DCI) remains the main cause of high mortality and morbidity in patients who survive the initial bleeding. Astrocytes play a key role in neurovascular coupling. Therefore, changes in the neurovascular unit including astrocytes following SAH may contribute to the development of DCI and long-term complications. In this study, we characterized morphological changes in hippocampal astrocytes following experimental SAH, with special emphasis on glia-vascular cross-talk and hippocampal volume changes. Four days after induction of SAH or sham-operation in mice, their hippocampal volumes were determined by magnetic resonance imaging (MRI) and histological/stereological methods. Glial fibrillary acid protein (GFAP) immunostained hippocampal sections were examined by stereological techniques to detect differences in astrocyte morphology, and global spatial sampling method was used to quantify the length density of Aquaporin-4 (AQP4) positive capillaries. Our results indicated that hippocampal volume, as measured both by MRI and by histological approaches, was significantly lower in SAH animals than in the sham-operated group. Accordingly, in this animal model of SAH, hippocampal atrophy existed already at the time of DCI onset in humans. SAH induced retraction of GFAP positive astrocyte processes, accompanied by a significant reduction in the length density of AQP4 positive capillaries as well as narrowing of hippocampal capillaries. Meanwhile, astrocyte volume was higher in SAH mice compared with the sham-operated group. Morphological changes in hippocampal astrocytes seemingly disrupt glia-vascular interactions early after SAH and may contribute to hippocampal atrophy. We speculate that astrocytes and astrocyte-capillary interactions may provide targets for the development of therapies to improve the prognosis of SAH.

Indexed as

aquaporin-4astrocytehippocampusMRIsubarachnoid hemorrhage

Identifiers

PMID29445328
PMCPMC5797792
OpenAlexW2794140100

What OpenQuestion holds

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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.