Evidence map›Paper›PMID 29042514›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Neuron-specific methylome analysis reveals epigenetic regulation and tau-related dysfunction of BRCA1 in Alzheimer's disease.

Tatsuo Mano, Kenichi Nagata, Takashi Nonaka, Airi Tarutani, Tomohiro Imamura, Tadafumi Hashimoto, Taro Bannai, Kagari Koshi-Mano, Takeyuki Tsuchida, Ryo Ohtomo and 13 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
3.9field-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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.

  1. The Role of c-Abl in Alzheimer's Disease: Guilty or not Guilty?Cellular and molecular neurobiology · 2025
    Pooled it
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. DNA Methylation in Alzheimer's Disease.Current topics in behavioral neurosciences · 2025
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. BRCA1 Promotes Repair of DNA Damage in Cochlear Hair Cells and Prevents Hearing Loss.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. ZNF714 Supports Pro-Oncogenic Features in Lung Cancer Cells.International journal of molecular sciences · 2023
    Article
  19. Review
  20. Article

1 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

23 authors at 9 institutions in 1 country.

Tatsuo ManoDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Kenichi NagataLaboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako-shi, Saitama 351-0198, Japan.
Takashi NonakaDepartment of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.ORCID 0000-0002-0830-9403
Airi TarutaniDepartment of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Tomohiro ImamuraDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Tadafumi HashimotoDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Taro BannaiDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Kagari Koshi-ManoDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Takeyuki TsuchidaDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Ryo OhtomoDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Junko Takahashi-FujigasakiDepartment of Neuropathology, Tokyo Metropolitan Geriatric Hospital, Tokyo 173-0015, Japan.
Satoshi YamashitaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Yasumasa OhyagiDepartment of Neurology and Geriatric Medicine, Ehime University Hospital, Shitsukawa, Toon, Ehime 791-0295, Japan.
Ryo YamasakiDepartment of Neurology, Neurological Institute, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Shoji TsujiDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Akira TamaokaDepartment of Neurology, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
Takeshi IkeuchiDepartment of Molecular Genetics, Brain Research Institute, Niigata University, Niigata 951-8585, Japan.
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Brain Science Institute, Wako-shi, Saitama 351-0198, Japan.
Takeshi IwatsuboDepartment of Neuropathology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Toshikazu UshijimaDivision of Epigenomics, National Cancer Center Research Institute, Tokyo 104-0045, Japan.
Shigeo MurayamaDepartment of Neuropathology, Tokyo Metropolitan Geriatric Hospital, Tokyo 173-0015, Japan.
Masato HasegawaDepartment of Dementia and Higher Brain Function, Tokyo Metropolitan Institute of Medical Science, Tokyo 156-8506, Japan.
Atsushi IwataDepartment of Neurology, Graduate School of Medicine, The University of Tokyo, Tokyo 113-8655, Japan; iwata@m.u-tokyo.ac.jp.ORCID 0000-0001-7308-5314
The University of Tokyo · JPTokyo Metropolitan Institute of Medical Science · JPKyushu University · JPRIKEN Center for Brain Science · JPTokyo Metropolitan Geriatric Hospital · JPEhime University Hospital · JPJapan Science and Technology Agency · JPNiigata University · JPUniversity of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a chronic neurodegenerative disease characterized by pathology of accumulated amyloid β (Aβ) and phosphorylated tau proteins in the brain. Postmortem degradation and cellular complexity within the brain have limited approaches to molecularly define the causal relationship between pathological features and neuronal dysfunction in AD. To overcome these limitations, we analyzed the neuron-specific DNA methylome of postmortem brain samples from AD patients, which allowed differentially hypomethylated region of the

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorAnimalsBrainBRCA1 ProteinDisease Models, AnimalDNA DamageDNA MethylationEpigenesis, GeneticHumansNeuronal PlasticityNeuronsPromoter Regions, GeneticSignal Transductiontau ProteinsAmyloid beta-PeptidesAmyloid beta-Protein PrecursorBRCA1 Proteintau ProteinsAlzheimer’s diseaseBRCA1DNA repairmethylome

Identifiers

PMID29042514
PMCPMC5692545
OpenAlexW2766547604

What OpenQuestion holds

Textmetadata
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.