Evidence map›Paper›PMID 38167174›Full record

ArticleActa neuropathologica communications2024

Histone acetylation in an Alzheimer's disease cell model promotes homeostatic amyloid-reducing pathways.

Daniel C Xu, Hanna Sas-Nowosielska, Greg Donahue, Hua Huang, Naemeh Pourshafie, Charly R Good, Shelley L Berger

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

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  12. Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024
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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

7 authors at 1 institution in 1 country.

Daniel C XuDepartment of Cell and Developmental Biology, Perelman School of Medicine Philadelphia, Penn Institute of Epigenetics, Philadelphia, PA, 19104, USA.
Hanna Sas-NowosielskaDepartment of Cell and Developmental Biology, Perelman School of Medicine Philadelphia, Penn Institute of Epigenetics, Philadelphia, PA, 19104, USA.
Greg DonahueDepartment of Cell and Developmental Biology, Perelman School of Medicine Philadelphia, Penn Institute of Epigenetics, Philadelphia, PA, 19104, USA.
Hua HuangDepartment of Cell and Developmental Biology, Perelman School of Medicine Philadelphia, Penn Institute of Epigenetics, Philadelphia, PA, 19104, USA.
Naemeh PourshafieDepartment of Cell and Developmental Biology, Perelman School of Medicine Philadelphia, Penn Institute of Epigenetics, Philadelphia, PA, 19104, USA.
Charly R GoodDepartment of Cell and Developmental Biology, Perelman School of Medicine Philadelphia, Penn Institute of Epigenetics, Philadelphia, PA, 19104, USA.
Shelley L BergerDepartment of Cell and Developmental Biology, Perelman School of Medicine Philadelphia, Penn Institute of Epigenetics, Philadelphia, PA, 19104, USA. bergers@pennmedicine.upenn.edu.ORCID 0000-0001-5398-4400
Penn Center for AIDS Research · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007170 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI BRASS, LAWRENCE F · 1985 to 2022
$54.0M
STRUCTURAL BASIS FOR EPIGENETICS IN AGING AND LONGEVITYP01AG031862 · NIA · WISTAR INSTITUTE · PI ZHANG, RUGANG · 2008 to 2022
$28.3M
The metabolic-epigenetic axis in memoryR01AA027202 · NIAAA · UNIVERSITY OF PENNSYLVANIA · PI BERGER, SHELLEY L · 2019 to 2023
$2.2M
NIAAA NIH HHS R01 AA027202NIA NIH HHS P01 AG031862NIGMS NIH HHS T32 GM007170Robert J. Kleberg, Jr. and Helen C. Kleberg Foundation Kleberg Foundation
6 · The paper itself

Abstract

Alzheimer's Disease (AD) is a disorder characterized by cognitive decline, neurodegeneration, and accumulation of amyloid plaques and tau neurofibrillary tangles in the brain. Dysregulation of epigenetic histone modifications may lead to expression of transcriptional programs that play a role either in protecting against disease genesis or in worsening of disease pathology. One such histone modification, acetylation of histone H3 lysine residue 27 (H3K27ac), is primarily localized to genomic enhancer regions and promotes active gene transcription. We previously discovered H3K27ac to be more abundant in AD patient brain tissue compared to the brains of age-matched non-demented controls. In this study, we use iPSC-neurons derived from familial AD patients with an amyloid precursor protein (APP) duplication (APP

Indexed as

Alzheimer DiseaseAcetylationAmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorHistonesHumanstau ProteinsAmyloidAmyloid beta-PeptidesAmyloid beta-Protein PrecursorHistonestau Proteins

Identifiers

PMID38167174
PMCPMC10759377
OpenAlexW4390501506

What Socratic 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 Socratic graph.