Evidence map›Paper›PMID 42845354›Full record

ArticlebioRxiv : the preprint server for biology2026

Juvenile influenza can impair myelin development and adult behavior through chemokine signaling in mice.

Karen Malacon, Kiarash Shamardani, Sophia Artandi, Lijun Ni, Natalia K Zernicka-Glover, Abigail Rogers, Belgin Yalçın, Enrique Herrera Castañeda, Theresa Pham, Akiko Iwasaki and 3 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. 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

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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.

No citing paper in PubMed yet.

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

13 authors.

Karen MalaconDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Kiarash ShamardaniDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Sophia ArtandiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Lijun NiDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Natalia K Zernicka-GloverDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Abigail RogersDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Belgin YalçınDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Enrique Herrera CastañedaDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Theresa PhamDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Akiko IwasakiDepartment of Immunobiology, Yale University, New Haven, CT 06520, USA.ORCID 0000-0002-7824-9856
Catherine A BlishDepartment of Medicine, Stanford University School of Medicine, Stanford, CA 94305, USA.
Anna C GeraghtyDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.
Michelle MonjeDepartment of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305, USA.

Funding

Early life influenza infection and glial dysregulationF31NS143332 · NINDS · STANFORD UNIVERSITY · PI Karen Elizabeth Malacon · 2025 to 2026
$100k
NINDS NIH HHS F31 NS143332
6 · The paper itself

Abstract

Brain development, especially developmental myelination, continues through young adulthood. Concordantly, children may be particularly vulnerable to neural-immune challenges. To investigate the consequences of major childhood immune challenges, juvenile mice were exposed to respiratory influenza (H1N1) infection. White matter-specific microglial reactivity accompanied by oligodendrocyte loss was evident until two months following infection. Mice exhibited hyperlocomotion and impaired attention, but not anxiety-like behavior, at one month following infection. Linking the oligodendroglial and behavioral deficits, genetic disruption of oligodendrocyte development at the same juvenile timepoint recapitulated this behavioral phenotype. Microglial reactivity and oligodendrocyte numbers normalized by young adulthood. However, myelin development was disrupted, with persistently decreased myelinated axon density and reduced myelin sheath thickness. Hyperlocomotion resolved, but anxiety-related behaviors emerged at two months after infection. At 6 months, anxiety resolved but cognitive deficits persisted. Elevated CSF chemokines and microglial chemokine expression prompted testing the role of the multi-chemokine receptor CCR3. CCR3 inhibition rescued these cellular and behavioral aberrations after juvenile H1N1 infection. Together, these findings underscore the potential for disruption of myelin development and lasting cognitive and neuropsychiatric sequelae following major immune challenges during the juvenile period and highlight chemokine signaling as an important therapeutic target.

Identifiers

PMID42845354
PMCPMC13640621

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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.