Evidence map›Paper›PMID 31804560›Full record

ArticleScientific reports2019

Common genetic variants associated with Parkinson's disease display widespread signature of epigenetic plasticity.

Amit Sharma, Naoki Osato, Hongde Liu, Shailendra Asthana, Tikam Chand Dakal, Giovanna Ambrosini, Philipp Bucher, Ina Schmitt, Ullrich Wüllner

Abstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Review
  5. An Overview of Epigenetic Changes in the Parkinson's Disease Brain.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Epigenetics of Aging and Aging-Associated Diseases.International journal of molecular sciences · 2021
    Review
  11. Review
  12. Review
  13. Parkinson's disease treatment: past, present, and future.Journal of neural transmission (Vienna, Austria : 1996) · 2020
    Review
  14. Article
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.

Amit SharmaDepartment of Neurology, University Clinic Bonn, Bonn, Germany.ORCID http://orcid.org/0000-0002-2216-5389
Naoki OsatoDepartment of Bioinformatics Engineering, Osaka University, Osaka, Japan.
Hongde LiuState Key Laboratory of Bioelectronics, Southeast University, Nanjing, China.
Shailendra AsthanaDrug Discovery Research Centre (DDRC), Translational Health Science and Technology Institute (THSTI), Haryana, 121001, India.
Tikam Chand DakalGenome & Computational Biology Lab, Department of Biotechnology, Mohanlal Sukhadia University, Udaipur, 313001, Rajasthan, India.
Giovanna AmbrosiniEPFL and Swiss Institute of Bioinformatics, Lausanne, Switzerland.
Philipp BucherEPFL and Swiss Institute of Bioinformatics, Lausanne, Switzerland.
Ina SchmittDepartment of Neurology, University Clinic Bonn, Bonn, Germany.
Ullrich WüllnerDepartment of Neurology, University Clinic Bonn, Bonn, Germany. ullrich.wuellner@ukbonn.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Parkinson disease (PD) is characterized by a pivotal progressive loss of substantia nigra dopaminergic neurons and aggregation of α-synuclein protein encoded by the SNCA gene. Genome-wide association studies identified almost 100 sequence variants linked to PD in SNCA. However, the consequences of this genetic variability are rather unclear. Herein, our analysis on selective single nucleotide polymorphisms (SNPs) which are highly associated with the PD susceptibility revealed that several SNP sites attribute to the nucleosomes and overlay with bivalent regions poised to adopt either active or repressed chromatin states. We also identified large number of transcription factor (TF) binding sites associated with these variants. In addition, we located two docking sites in the intron-1 methylation prone region of SNCA which are required for the putative interactions with DNMT1. Taken together, our analysis reflects an additional layer of epigenomic contribution for the regulation of the SNCA gene in PD.

Indexed as

Epigenesis, Geneticalpha-SynucleinBinding SitesChromatinDatasets as TopicDNA (Cytosine-5-)-Methyltransferase 1DNA MethylationDopaminergic NeuronsGenetic Predisposition to DiseaseGenome-Wide Association StudyHistonesHumansIntronsNucleosomesParkinson DiseasePolymorphism, Single Nucleotidealpha-SynucleinChromatinDNA (Cytosine-5-)-Methyltransferase 1DNMT1 protein, humanHistonesNucleosomesSNCA protein, human

Identifiers

PMID31804560
PMCPMC6895091

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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.