Evidence map›Paper›PMID 38328164›Full record

ArticlebioRxiv : the preprint server for biology2024

Neuroinflammation underlies the development of social stress induced cognitive deficit in sickle cell disease.

S'Dravious A DeVeaux, Sofiya Vyshnya, Katherine Propsom, Oluwabukola T Gbotosho, Asem S Singh, Robert Z Horning, Mihika Sharma, Anil G Jegga, Liang Niu, Edward A Botchwey and 1 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 1 country.

S'Dravious A DeVeauxThe Wallace H. Coulter Department of Biomedical Engineering, Georgia Tech and Emory, Atlanta, GA, USA.
Sofiya VyshnyaThe Wallace H. Coulter Department of Biomedical Engineering, Georgia Tech and Emory, Atlanta, GA, USA.
Katherine PropsomDepartment of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Oluwabukola T GbotoshoDepartment of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Asem S SinghDepartment of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Robert Z HorningDepartment of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Mihika SharmaDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine Cincinnati, OH, USA.
Anil G JeggaDivision of Biomedical Informatics, Cincinnati Children's Hospital Medical Center, Department of Pediatrics, University of Cincinnati College of Medicine Cincinnati, OH, USA.
Liang NiuDepartment of Environmental and Public Health Sciences, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Edward A BotchweyThe Wallace H. Coulter Department of Biomedical Engineering, Georgia Tech and Emory, Atlanta, GA, USA.ORCID 0000-0003-1140-5786
Hyacinth I HyacinthDepartment of Neurology and Rehabilitation Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.ORCID 0000-0002-1991-7463
University of Cincinnati Medical Center · USGeorgia Institute of Technology · USCincinnati Children's Hospital Medical Center · US

Funding

Sickle cell disease and the functional circuit of adult-born neurons in the dentate gyrusR01HL156024 · NHLBI · UNIVERSITY OF CINCINNATI · PI HYACINTH, HYACINTH IDU · 2021 to 2025
$4.0M
Mechanism of cerebral vaculopathy and stroke in sickle cell diseaseR01HL138423 · NHLBI · UNIVERSITY OF CINCINNATI · PI HYACINTH, HYACINTH IDU · 2017 to 2021
$2.5M
T32 CTEng (Cellular and Tissue Engineering) Training ProgramT32GM145735 · NIGMS · GEORGIA INSTITUTE OF TECHNOLOGY · PI Edward A. Botchwey, Andres J Garcia · 2022 to 2026
$2.3M
NHLBI NIH HHS R01 HL138423NHLBI NIH HHS R01 HL156024NIGMS NIH HHS T32 GM145735
6 · The paper itself

Abstract

Cognitive deficit is a debilitating complication of SCD with multifactorial pathobiology. Here we show that neuroinflammation and dysregulation in lipidomics and transcriptomics profiles are major underlying mechanisms of social stress-induced cognitive deficit in SCD. Townes sickle cell (SS) mice and controls (AA) were exposed to social stress using the repeat social defeat (RSD) paradigm concurrently with or without treatment with minocycline. Mice were tested for cognitive deficit using novel object recognition (NOR) and fear conditioning (FC) tests. SS mice exposed to RSD without treatment had worse performance on cognitive tests compared to SS mice exposed to RSD with treatment or to AA controls, irrespective of their RSD or treatment disposition. Additionally, compared to SS mice exposed to RSD with treatment, SS mice exposed to RSD without treatment had significantly more cellular evidence of neuroinflammation coupled with a significant shift in the differentiation of neural progenitor cells towards astrogliogenesis. Additionally, brain tissue from SS mice exposed to RSD was significantly enriched for genes associated with blood-brain barrier dysfunction, neuron excitotoxicity, inflammation, and significant dysregulation in sphingolipids important to neuronal cell processes. We demonstrate in this study that neuroinflammation and lipid dysregulation are potential underlying mechanisms of social stress-related cognitive deficit in SS mice.

Identifiers

PMID38328164
PMCPMC10849745
OpenAlexW4391238628

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.