Evidence map›Paper›PMID 28700589›Full record

ArticlePloS one2017

ANK1 is up-regulated in laser captured microglia in Alzheimer's brain; the importance of addressing cellular heterogeneity.

Diego Mastroeni, Shobana Sekar, Jennifer Nolz, Elaine Delvaux, Katie Lunnon, Jonathan Mill, Winnie S Liang, Paul D Coleman

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 3 pooled it
3.4field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 3 syntheses or guidelines pooled it, 47 citations in OpenAlex.

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  4. Epigenetics in Neurodegenerative Diseases.Sub-cellular biochemistry · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Diego MastroeniBiodesign, ASU-Banner Biodesign Neurodegenerative Disease Research Center, and School of Life Sciences, Arizona State University, Tempe, AZ, United States of America.ORCID http://orcid.org/0000-0001-5878-9372
Shobana SekarTranslational Genomics Institute, 445 North Fifth Street, Phoenix, AZ, United States of America.
Jennifer NolzBiodesign, ASU-Banner Biodesign Neurodegenerative Disease Research Center, and School of Life Sciences, Arizona State University, Tempe, AZ, United States of America.
Elaine DelvauxBiodesign, ASU-Banner Biodesign Neurodegenerative Disease Research Center, and School of Life Sciences, Arizona State University, Tempe, AZ, United States of America.
Katie LunnonUniversity of Exeter Medical School, RILD, University of Exeter, Devon, United Kingdom.
Jonathan MillUniversity of Exeter Medical School, RILD, University of Exeter, Devon, United Kingdom.
Winnie S LiangTranslational Genomics Institute, 445 North Fifth Street, Phoenix, AZ, United States of America.
Paul D ColemanBiodesign, ASU-Banner Biodesign Neurodegenerative Disease Research Center, and School of Life Sciences, Arizona State University, Tempe, AZ, United States of America.
Arizona State University · USBanner Sun Health Research Institute · USTranslational Genomics Research Institute · USKing's College London · GBUniversity of Exeter · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Recent epigenetic association studies have identified a new gene, ANK1, in the pathogenesis of Alzheimer's disease (AD). Although strong associations were observed, brain homogenates were used to generate the data, introducing complications because of the range of cell types analyzed. In order to address the issue of cellular heterogeneity in homogenate samples we isolated microglial, astrocytes and neurons by laser capture microdissection from CA1 of hippocampus in the same individuals with a clinical and pathological diagnosis of AD and matched control cases. Using this unique RNAseq data set, we show that in the hippocampus, ANK1 is significantly (p<0.0001) up-regulated 4-fold in AD microglia, but not in neurons or astrocytes from the same individuals. These data provide evidence that microglia are the source of ANK1 differential expression previously identified in homogenate samples in AD.

Indexed as

Up-RegulationAgedAged, 80 and overAlzheimer DiseaseAnkyrinsCase-Control StudiesFemaleHippocampusHumansMaleMicrogliaNeuronsRNA, MessengerANK1 protein, humanAnkyrinsRNA, Messenger

Identifiers

PMID28700589
PMCPMC5507536
OpenAlexW2735096048

What OpenQuestion holds

Textmetadata
LicenceCC0
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.