Evidence map›Paper›PMID 32419307›Full record

ArticleAging cell2020

Epigenome signatures landscaped by histone H3K9me3 are associated with the synaptic dysfunction in Alzheimer's disease.

Min Young Lee, Junghee Lee, Seung Jae Hyeon, Hyesun Cho, Yu Jin Hwang, Jong-Yeon Shin, Ann C McKee, Neil W Kowall, Jong-Il Kim, Thor D Stein and 2 more

Open access · goldAbstract read
In one paragraph

Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.

  1. Systematic review and meta-analysis of bulk RNAseq studies in human Alzheimer's disease brain tissue.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Physical models reveal indirect reader protein interactions that facilitate epigenetic crosstalk.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. Article
  11. Review
  12. Epigenetics in Neurodegenerative Diseases.Sub-cellular biochemistry · 2025
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Physical modeling of nucleosome clustering in euchromatin resulting from interactions between epigenetic reader proteins.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  18. Article
  19. Article
  20. Review
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

12 authors at 4 institutions in 2 countries.

Min Young LeeInstitute for Systems Biology, Seattle, WA, USA.
Junghee LeeVeteran's Affairs Boston Healthcare System, Boston, MA, USA.
Seung Jae HyeonCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, South Korea.
Hyesun ChoGenome Medicine Institute and Department of Biochemistry, Seoul National University College of Medicine, Seoul, South Korea.
Yu Jin HwangCenter for Neuromedicine, Brain Science Institute, Korea Institute of Science and Technology, Seoul, South Korea.
Jong-Yeon ShinGenome Medicine Institute and Department of Biochemistry, Seoul National University College of Medicine, Seoul, South Korea.
Ann C McKeeVeteran's Affairs Boston Healthcare System, Boston, MA, USA.
Neil W KowallVeteran's Affairs Boston Healthcare System, Boston, MA, USA.
Jong-Il KimGenome Medicine Institute and Department of Biochemistry, Seoul National University College of Medicine, Seoul, South Korea.
Thor D SteinVeteran's Affairs Boston Healthcare System, Boston, MA, USA.
Daehee HwangDepartment of Biological Sciences, Seoul National University, Seoul, South Korea.
Hoon RyuVeteran's Affairs Boston Healthcare System, Boston, MA, USA.ORCID 0000-0001-6544-3732
Boston University · USSeoul National University · KRKorea Institute of Brain Science · KRInstitute for Systems Biology · US

Funding

Age-Associated Lipidomic Changes in Alzheimer's DiseaseRF1AG057768 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI BLUSZTAJN, JAN KRZYSZTOF, STEIN, THOR · 2019 to 2021
$4.5M
Tau Pathology in CTE vs. Alzheimer's Disease: Microvasculopathy and NeuroinflammationRF1AG057902 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2017 to 2017
$4.1M
Epigenetic changes in synaptic and inflammatory genes involved in the age-dependent development of Alzheimer's disease pathologies andcognitive declineRF1AG054156 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI AU, RHODA, RYU, HOON · 2016 to 2018
$3.4M
Modulation of neuronal atrophy in Huntington's diseaseR01NS109537 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LEE, JUNGHEE · 2018 to 2022
$1.4M
Epigenetic Regulation of Heterochromatin Condensation in Huntington's DiseaseR01NS067283 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RYU, HOON · 2011 to 2015
$1.2M
NIA NIH HHS RF1 AG054156NIA NIH HHS RF1 AG057768NIA NIH HHS RF1 AG057902NIH HHS R01NS067283NINDS NIH HHS R01 NS109537
6 · The paper itself

Abstract

The pathogenesis of Alzheimer's disease (AD) and the commonest cause of dementia in the elderly remain incompletely understood. Recently, epigenetic modifications have been shown to play a potential role in neurodegeneration, but the specific involvement of epigenetic signatures landscaped by heterochromatin has not been studied in AD. Herein, we discovered that H3K9me3-mediated heterochromatin condensation is elevated in the cortex of sporadic AD postmortem brains. In order to identify which epigenomes are modulated by heterochromatin, we performed H3K9me3-chromatin immunoprecipitation (ChIP)-sequencing and mRNA-sequencing on postmortem brains from normal subjects and AD patients. The integrated analyses of genome-wide ChIP- and mRNA-sequencing data identified epigenomes that were highly occupied by H3K9me3 and inversely correlated with their mRNA expression levels in AD. Biological network analysis further revealed H3K9me3-landscaped epigenomes to be mainly involved in synaptic transmission, neuronal differentiation, and cell motility. Together, our data show that the abnormal heterochromatin remodeling by H3K9me3 leads to down-regulation of synaptic function-related genes, suggesting that the epigenetic alteration by H3K9me3 is associated with the synaptic pathology of sporadic AD.

Indexed as

Alzheimer DiseaseEpigenomeHistonesHumansSynaptic TransmissionHistonesAlzheimer's diseaseepigenetic modificationsgenome-wide sequencinghistone H3K9me3synaptic transmission

Identifiers

PMID32419307
PMCPMC7294781
OpenAlexW3024012994

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.