Evidence map›Paper›PMID 33083725›Full record

ArticleiScience2020

Spatial Transcriptomics Reveals Genes Associated with Dysregulated Mitochondrial Functions and Stress Signaling in Alzheimer Disease.

José Fernández Navarro, Deborah L Croteau, Aleksandra Jurek, Zaneta Andrusivova, Beimeng Yang, Yue Wang, Benjamin Ogedegbe, Tahira Riaz, Mari Støen, Claus Desler and 5 more

Abstract read
In one paragraph

Article in iScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 1 pooled it
–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

75 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  19. Phosphorylation of Bok at Ser-8 blocks its ability to suppress IPCell communication and signaling : CCS · 2025
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15 more citing papers are in PubMed but not listed here.

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

15 authors.

José Fernández NavarroScience for Life Laboratory, Department of Gene Technology, KTH Royal Institute of Technology, 17165 Stockholm, Sweden.
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, Baltimore, MD 21224, USA.
Aleksandra JurekScience for Life Laboratory, Department of Gene Technology, KTH Royal Institute of Technology, 17165 Stockholm, Sweden.
Zaneta AndrusivovaScience for Life Laboratory, Department of Gene Technology, KTH Royal Institute of Technology, 17165 Stockholm, Sweden.
Beimeng YangLaboratory of Molecular Gerontology, National Institute on Aging, Baltimore, MD 21224, USA.
Yue WangLaboratory of Molecular Gerontology, National Institute on Aging, Baltimore, MD 21224, USA.
Benjamin OgedegbeLaboratory of Molecular Gerontology, National Institute on Aging, Baltimore, MD 21224, USA.
Tahira RiazUnit for Genome Dynamics, Department of Microbiology, University of Oslo and Oslo University Hospital, 0372 Oslo, Norway.
Mari StøenUnit for Genome Dynamics, Department of Microbiology, University of Oslo and Oslo University Hospital, 0372 Oslo, Norway.
Claus DeslerCenter for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, 2200 Copenhagen, Denmark.
Lene Juel RasmussenCenter for Healthy Aging, Department of Cellular and Molecular Medicine, University of Copenhagen, 2200 Copenhagen, Denmark.
Tone TønjumUnit for Genome Dynamics, Department of Microbiology, University of Oslo and Oslo University Hospital, 0372 Oslo, Norway.
Marie-Christine GalasUniversity of Lille, Inserm, CHU Lille, UMR-S 1172 - Centre de Recherche Jean-Pierre AUBERT Neurosciences et Cancer, 59000 Lille, France.
Joakim LundebergScience for Life Laboratory, Department of Gene Technology, KTH Royal Institute of Technology, 17165 Stockholm, Sweden.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, Baltimore, MD 21224, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer disease (AD) is a devastating neurological disease associated with progressive loss of mental skills and cognitive and physical functions whose etiology is not completely understood. Here, our goal was to simultaneously uncover novel and known molecular targets in the structured layers of the hippocampus and olfactory bulbs that may contribute to early hippocampal synaptic deficits and olfactory dysfunction in AD mice. Spatially resolved transcriptomics was used to identify high-confidence genes that were differentially regulated in AD mice relative to controls. A diverse set of genes that modulate stress responses and transcription were predominant in both hippocampi and olfactory bulbs. Notably, we identify Bok, implicated in mitochondrial physiology and cell death, as a spatially downregulated gene in the hippocampus of mouse and human AD brains. In summary, we provide a rich resource of spatially differentially expressed genes, which may contribute to understanding AD pathology.

Indexed as

Cellular NeuroscienceOmicsTranscriptomics

Identifiers

PMID33083725
PMCPMC7522123

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.