Evidence map›Paper›PMID 18628954›Full record

ArticlePloS one2008

Age-specific epigenetic drift in late-onset Alzheimer's disease.

Sun-Chong Wang, Beatrice Oelze, Axel Schumacher

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

Article in PloS one, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed, 3 pooled it
13.1field-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

203 citing papers in PubMed, 3 syntheses or guidelines pooled it, 467 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Trial
  5. Epigenetic changes in the progression of Alzheimer's disease.Mechanisms of ageing and development · 2013
    Trial
  6. Trial
  7. Article
  8. Advances in the treatment of Alzheimer's disease.Frontiers in pharmacology · 2026
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. DNA Methylation in Alzheimer's Disease.Current topics in behavioral neurosciences · 2025
    Review
  16. Review
  17. Review
  18. Article
  19. Epigenetics in Alzheimer's Disease: A Critical Overview.International journal of molecular sciences · 2024
    Review
  20. Review

143 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

3 authors at 2 institutions in 2 countries.

Sun-Chong WangInstitute of Systems Biology and Bioinformatics, National Central University, Jhongli City, Taiwan.
Beatrice Oelze
Axel Schumacher
Klinikum rechts der Isar · DENational Central University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite an enormous research effort, most cases of late-onset Alzheimer's disease (LOAD) still remain unexplained and the current biomedical science is still a long way from the ultimate goal of revealing clear risk factors that can help in the diagnosis, prevention and treatment of the disease. Current theories about the development of LOAD hinge on the premise that Alzheimer's arises mainly from heritable causes. Yet, the complex, non-Mendelian disease etiology suggests that an epigenetic component could be involved. Using MALDI-TOF mass spectrometry in post-mortem brain samples and lymphocytes, we have performed an analysis of DNA methylation across 12 potential Alzheimer's susceptibility loci. In the LOAD brain samples we identified a notably age-specific epigenetic drift, supporting a potential role of epigenetic effects in the development of the disease. Additionally, we found that some genes that participate in amyloid-beta processing (PSEN1, APOE) and methylation homeostasis (MTHFR, DNMT1) show a significant interindividual epigenetic variability, which may contribute to LOAD predisposition. The APOE gene was found to be of bimodal structure, with a hypomethylated CpG-poor promoter and a fully methylated 3'-CpG-island, that contains the sequences for the epsilon4-haplotype, which is the only undisputed genetic risk factor for LOAD. Aberrant epigenetic control in this CpG-island may contribute to LOAD pathology. We propose that epigenetic drift is likely to be a substantial mechanism predisposing individuals to LOAD and contributing to the course of disease.

Indexed as

Epigenesis, GeneticAgedAged, 80 and overAge FactorsAlzheimer DiseaseAmyloid beta-PeptidesCpG IslandsDNA MethylationFemaleHaplotypesHomeostasisHumansMaleModels, GeneticSpectrometry, Mass, Matrix-Assisted Laser Desorption-IonizationAmyloid beta-Peptides

Identifiers

PMID18628954
PMCPMC2444024
OpenAlexW2020089910

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.