Evidence map›Paper›PMID 35203383›Full record

ArticleCells2022

Histone H3 Lysine 4 and 27 Trimethylation Landscape of Human Alzheimer's Disease.

Giuseppe Persico, Francesca Casciaro, Stefano Amatori, Martina Rusin, Francesco Cantatore, Amalia Perna, Lavinia Alberi Auber, Mirco Fanelli, Marco Giorgio

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

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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

9 authors at 5 institutions in 3 countries.

Giuseppe PersicoDepartment of Experimental Oncology, IRCCS-European Institute of Oncology, Via Adamello 16, 20139 Milano, Italy.
Francesca CasciaroDepartment of Biomedical Sciences, University of Padua, Via Ugo Bassi 58/B, 35131 Padova, Italy.ORCID 0000-0002-1404-6099
Stefano AmatoriMolecular Pathology Laboratory "PaoLa", Department of Biomolecular Sciences, University of Urbino Carlo Bo, Via Arco d'Augusto 2, 61032 Fano (PU), Italy.ORCID 0000-0003-3988-3480
Martina RusinDepartment of Experimental Oncology, IRCCS-European Institute of Oncology, Via Adamello 16, 20139 Milano, Italy.ORCID 0000-0002-3012-2653
Francesco CantatoreMolecular Pathology Laboratory "PaoLa", Department of Biomolecular Sciences, University of Urbino Carlo Bo, Via Arco d'Augusto 2, 61032 Fano (PU), Italy.ORCID 0000-0002-2078-0206
Amalia PernaDepartment of Pathology, School of Medicine, Stanford University, 300 Pasteur Drive, Stanford, CA 94305, USA.
Lavinia Alberi AuberSwiss Integrative Center of Human Health, Pass. du Cardinal 13, 1700 Fribourg, Switzerland.ORCID 0000-0002-0446-5337
Mirco FanelliMolecular Pathology Laboratory "PaoLa", Department of Biomolecular Sciences, University of Urbino Carlo Bo, Via Arco d'Augusto 2, 61032 Fano (PU), Italy.ORCID 0000-0002-9649-8661
Marco GiorgioDepartment of Experimental Oncology, IRCCS-European Institute of Oncology, Via Adamello 16, 20139 Milano, Italy.
University of Urbino · ITUniversity of Padua · ITEuropean Institute of Oncology · ITStanford University · USUniversity of Fribourg · CH

Funding

A ketogenic longevity diet for resistance to age-related functional decline and Alzheimer's diseaseR56AG057163 · NIA · UNIVERSITY OF CALIFORNIA AT DAVIS · PI CORTOPASSI, GINO A, RAMSEY, JON J. · 2018 to 2018
$783k
NIH HHS 1R56AG057163-01A1
6 · The paper itself

Abstract

backgroundEpigenetic remodeling is emerging as a critical process for both the onset and progression of Alzheimer's disease (AD), the most common form of neurodegenerative dementia. However, it is not clear to what extent the distribution of histone modifications is involved in AD.

methodsTo investigate histone H3 modifications in AD, we compared the genome-wide distributions of H3K4me3 and H3K27me3 in entorhinal cortices from severe sporadic AD patients and from age-matched healthy individuals of both sexes.

resultsAD samples were characterized by typical average levels and distributions of the H3K4me3 and H3K27me3 signals. However, AD patients showed a lower H3K4me3 and higher H3K27me3 signal, particularly in males. Interestingly, the genomic sites found differentially trimethylated at the H3K4 between healthy and AD samples involve promoter regions of genes belonging to AD-related pathways such as glutamate receptor signaling.

conclusionsThe signatures of H3K4me3 and H3K27me3 identified in AD patients validate the role of epigenetic chromatin remodeling in neurodegenerative disease and shed light on the genomic adaptive mechanisms involved in AD.

Indexed as

Alzheimer DiseaseNeurodegenerative DiseasesEpigenesis, GeneticFemaleHistonesHumansLysineMaleMethylationPromoter Regions, GeneticHistonesLysineAlzheimer’s diseasechromatinhistone modificationsneuronal functions

Identifiers

PMID35203383
PMCPMC8870338
OpenAlexW4213219935

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.