Evidence map›Paper›PMID 38853870›Full record

ArticlebioRxiv : the preprint server for biology2024

A glial circadian gene expression atlas reveals cell type and disease-specific reprogramming in response to amyloid pathology or aging.

Patrick W Sheehan, Stuart Fass, Darshan Sapkota, Sylvia Kang, Henry C Hollis, Jennifer H Lawrence, Ron C Anafi, Joseph D Dougherty, Jon D Fryer, Erik S Musiek

Abstract readPreprint
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.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Patrick W SheehanDepartment of Neurology, Washington University School of Medicine, Saint Louis MO, USA.ORCID 0000-0001-8476-6246
Stuart FassDepartment of Genetics, Washington University School of Medicine, Saint Louis MO, USA.
Darshan SapkotaDepartment of Genetics, Washington University School of Medicine, Saint Louis MO, USA.ORCID 0000-0003-3773-2910
Sylvia KangDepartment of Neuroscience, Mayo Clinic, Jacksonville, FL, USA.
Henry C HollisSchool of Biomedical Engineering and Health Systems, Drexel University, Philadelphia, PA, USA.
Jennifer H LawrenceDepartment of Neurology, Washington University School of Medicine, Saint Louis MO, USA.ORCID 0000-0002-3501-7262
Ron C AnafiDepartment of Medicine, Chronobiology, and Sleep Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Joseph D DoughertyDepartment of Genetics, Washington University School of Medicine, Saint Louis MO, USA.ORCID 0000-0002-6385-3997
Jon D FryerDepartment of Neuroscience, Mayo Clinic, Scottsdale, AZ, USA.ORCID 0000-0003-3390-2994
Erik S MusiekDepartment of Neurology, Washington University School of Medicine, Saint Louis MO, USA.ORCID 0000-0002-8873-0360

Funding

ROLE OF GLIAL CIRCADIAN CLOCK DYSFUNCTION IN THE PATHOGENESIS OF ALZHEIMER'S DISEASER01AG054517 · NIA · WASHINGTON UNIVERSITY · PI Erik Steven Musiek · 2017 to 2026
$4.5M
Regulation of local translation in gliaR01NS102272 · NINDS · WASHINGTON UNIVERSITY · PI JOSEPH D DOUGHERTY · 2017 to 2026
$3.8M
Multidisciplinary Training in Alzheimer and Related DementiasT32AG058518 · NIA · WASHINGTON UNIVERSITY · PI Eric Martin McDade, Barbara Joy Snider · 2018 to 2026
$2.3M
Circadian Organization and Disorder in Alzheimer's DiseaseR01AG068577 · NIA · UNIVERSITY OF PENNSYLVANIA · PI ANAFI, RON C. · 2020 to 2024
$2.0M
Neurobiological significance of Aqp4 stop codon readthroughR00AG061231 · NIA · UNIVERSITY OF TEXAS DALLAS · PI SAPKOTA, DARSHAN · 2021 to 2023
$722k
NIA NIH HHS R00 AG061231NIA NIH HHS R01 AG054517NIA NIH HHS R01 AG068577NIA NIH HHS T32 AG058518NINDS NIH HHS R01 NS102272
6 · The paper itself

Abstract

While circadian rhythm disruption may promote neurodegenerative disease, how aging and neurodegenerative pathology impact circadian gene expression patterns in different brain cell types is unknown. Here, we used translating ribosome affinity purification methods to define the circadian translatomes of astrocytes, microglia, and bulk cerebral cortex, in healthy mouse brain and in the settings of amyloid-beta plaque pathology or aging. Our data reveal that glial circadian translatomes are highly cell type-specific and exhibit profound, context-dependent reprogramming of rhythmic transcripts in response to amyloid pathology or aging. Transcripts involved in glial activation, immunometabolism, and proteostasis, as well as nearly half of all Alzheimer Disease (AD)-associated risk genes, displayed circadian oscillations, many of which were altered by pathology. Amyloid-related differential gene expression was also dependent on time of day. Thus, circadian rhythms in gene expression are cell- and context dependent and provide important insights into glial gene regulation in health, AD, and aging.

Indexed as

agingAlzheimer’s Diseaseastrocytecircadiangliamicrogliatranscriptome

Identifiers

PMID38853870
PMCPMC11160685

What OpenQuestion holds

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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.