Evidence map›Paper›PMID 25201696›Full record

ArticleNeuropathology and applied neurobiology2015

Alterations in global DNA methylation and hydroxymethylation are not detected in Alzheimer's disease.

Tammaryn Lashley, Priya Gami, Navid Valizadeh, Abi Li, Tamas Revesz, Robert Balazs

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuropathology and applied neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 2 pooled it
–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

46 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. DNA Methylation in Alzheimer's Disease.Current topics in behavioral neurosciences · 2025
    Review
  9. Review
  10. Review
  11. Novel therapeutic approaches to target neurodegeneration.British journal of pharmacology · 2023
    Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Epigenetic Biomarkers as Diagnostic Tools for Neurodegenerative Disorders.International journal of molecular sciences · 2021
    Article
  19. Review
  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

6 authors.

Tammaryn LashleyQueen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Priya GamiQueen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Navid ValizadehQueen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Abi LiReta Lila Weston Research Laboratories and Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Tamas ReveszQueen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
Robert BalazsQueen Square Brain Bank for Neurological Disorders, Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsGenetic factors do not seem to account fully for Alzheimer disease (AD) pathogenesis. There is evidence for the contribution of environmental factors, whose effect may be mediated by epigenetic mechanisms. Epigenetics involves the regulation of gene expression independently of DNA sequence and these epigenetic changes are influenced by age and environmental factors, with DNA methylation being one of the best characterized epigenetic mechanisms. The human genome is predominantly methylated on CpG motifs, which results in gene silencing; however methylation within the body of the gene may mark active transcription. There is evidence suggesting an involvement of environmental factors in the pathogenesis of Alzheimer's disease (AD), which prompted our study examining DNA methylation in this disorder.

methodsUsing immunohistochemistry with 5-methylcytosine/5-hydroxymethylcytosine antibodies we studied, in comparison with age matched controls, DNA methylation in sporadic and familial AD cases in the entorhinal cortex that exhibits substantial pathology and the cerebellum, which is relatively spared.

resultsNeuronal nuclear labelling with 5-methylcytosine (5mC) and 5-hydroxymethylcytosine (5hmC) was evident in all cases studied. We did not detect any significant change in the levels of nuclear staining in the AD samples compared to neurologically normal controls. In the entorhinal cortex we also examined global DNA methylation and hydroxymethylation using an enzyme-linked immunosorbent assay (ELISA).

conclusionNo significant differences were found between AD and control cases in global levels of 5mC and 5hmC in the entorhinal cortex using immunohistochemistry and enzyme-linked immunosorbent assays.

Indexed as

DNA MethylationEpigenesis, Genetic5-MethylcytosineAdultAgedAged, 80 and overAlzheimer DiseaseCytosineEntorhinal CortexFemaleHumansMaleMiddle Aged5-hydroxymethylcytosine5-MethylcytosineCytosineAlzheimer's diseaseepigeneticshydroxymethylationmethylation

Identifiers

PMID25201696
PMCPMC4879505

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Registered trials

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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.