Evidence map›Paper›PMID 32424276›Full record

ArticleNature communications2020

HDAC1 modulates OGG1-initiated oxidative DNA damage repair in the aging brain and Alzheimer's disease.

Ping-Chieh Pao, Debasis Patnaik, L Ashley Watson, Fan Gao, Ling Pan, Jun Wang, Chinnakkaruppan Adaikkan, Jay Penney, Hugh P Cam, Wen-Chin Huang and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.

0numbers the graph read from it
0cells of the map it votes in
136citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

136 citing papers in PubMed, 204 citations in OpenAlex.

  1. Research progress on lysine acetylation (Review).International journal of molecular medicine · 2026
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  3. Simvastatin rescues cognitive impairment in an AβNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  10. Cellular senescence and aging: molecular mechanisms and convergent pathways.Cellular and molecular life sciences : CMLS · 2026
    Review
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  12. Review
  13. Review
  14. Review
  15. Article
  16. Review
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  18. Article
  19. Intermittent Fasting Enhances Genome Integrity and Cytoprotective Pathways via (BHB) β-Hydroxybutyrate Signaling and Chromatin Remodeling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  20. Article

76 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

18 authors at 6 institutions in 1 country.

Ping-Chieh PaoPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.ORCID http://orcid.org/0000-0001-6788-7185
Debasis Patnaik *Chemical Neurobiology Laboratory, Departments of Neurology and Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.ORCID http://orcid.org/0000-0002-9829-3352
L Ashley Watson *Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Fan GaoPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Ling PanPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Jun WangPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Chinnakkaruppan AdaikkanPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Jay PenneyPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Hugh P CamPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Wen-Chin HuangPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Lorena PantanoPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.ORCID http://orcid.org/0000-0002-3859-3249
Audrey LeePicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Alexi NottPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.ORCID http://orcid.org/0000-0002-2029-7193
Trongha X PhanPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Elizabeta GjoneskaPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Sara ElmsaouriPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Stephen J HaggartyChemical Neurobiology Laboratory, Departments of Neurology and Psychiatry, Massachusetts General Hospital and Harvard Medical School, Boston, MA, 02114, USA.ORCID http://orcid.org/0000-0002-7872-168X
Li-Huei TsaiPicower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. lhtsai@mit.edu.ORCID http://orcid.org/0000-0003-1262-0592
Massachusetts Institute of Technology · USHarvard University · USCalifornia Institute of Technology · USMcGovern Institute for Brain Research · USNational Institutes of Health · USUniversity of California San Diego · US

Funding

Targeting a Novel Regulator of Brain Aging and Alzheimer's Disease (ADMINISTRATIVE SUPPLEMENT- SAGE)R01AG046174 · NIA · HARVARD MEDICAL SCHOOL · PI TSAI, LI-HUEI, YANKNER, BRUCE A · 2014 to 2018
$4.9M
Mechanisms underlying DNA double strand break response in Alzheimer?s disease and frontal temporal dementiaR01NS102730 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI TSAI, LI-HUEI · 2017 to 2021
$2.1M
NIA NIH HHS R01 AG046174NINDS NIH HHS R01 NS102730
6 · The paper itself

Abstract

DNA damage contributes to brain aging and neurodegenerative diseases. However, the factors stimulating DNA repair to stave off functional decline remain obscure. We show that HDAC1 modulates OGG1-initated 8-oxoguanine (8-oxoG) repair in the brain. HDAC1-deficient mice display age-associated DNA damage accumulation and cognitive impairment. HDAC1 stimulates OGG1, a DNA glycosylase known to remove 8-oxoG lesions that are associated with transcriptional repression. HDAC1 deficiency causes impaired OGG1 activity, 8-oxoG accumulation at the promoters of genes critical for brain function, and transcriptional repression. Moreover, we observe elevated 8-oxoG along with reduced HDAC1 activity and downregulation of a similar gene set in the 5XFAD mouse model of Alzheimer's disease. Notably, pharmacological activation of HDAC1 alleviates the deleterious effects of 8-oxoG in aged wild-type and 5XFAD mice. Our work uncovers important roles for HDAC1 in 8-oxoG repair and highlights the therapeutic potential of HDAC1 activation to counter functional decline in brain aging and neurodegeneration.

Indexed as

DNA DamageOxidative StressAcetylationAgingAlzheimer DiseaseAnimalsAstrocytesBase SequenceBenzophenonesBrainCognitionCognition DisordersDNA GlycosylasesDown-RegulationGene OntologyGuanine8-hydroxyguanineBenzophenonesDNA GlycosylasesexifoneGuanineHdac1 protein, mouseHistone Deacetylase 1Ogg1 protein, mouse

Identifiers

PMID32424276
PMCPMC7235043
OpenAlexW3025772309

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.