Evidence map›Paper›PMID 33082299›Full record

ArticleAging2020

Hippocampal and cortical tissue-specific epigenetic clocks indicate an increased epigenetic age in a mouse model for Alzheimer's disease.

Emma Coninx, Yap Ching Chew, Xiaojing Yang, Wei Guo, Amelie Coolkens, Sarah Baatout, Lieve Moons, Mieke Verslegers, Roel Quintens

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

33 citing papers in PubMed, 44 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Leveraging Single-Cell RNA-Seq to Generate Robust Microglia Aging Clocks.bioRxiv : the preprint server for biology · 2024
    Article
  15. Review
  16. Article
  17. Epigenetics in Alzheimer's Disease: A Critical Overview.International journal of molecular sciences · 2024
    Review
  18. Article
  19. Article
  20. 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 at 2 institutions in 1 country.

Emma ConinxRadiobiology Unit, Institute for Environment, Health and Safety, Belgian Nuclear Research Centre (SCK CEN), Mol 2400, Belgium.
Yap Ching ChewEpigenetics Technologies, Zymo Research Corporation, Irvine, CA 92614, USA.
Xiaojing YangEpigenetics Technologies, Zymo Research Corporation, Irvine, CA 92614, USA.
Wei GuoEpigenetics Technologies, Zymo Research Corporation, Irvine, CA 92614, USA.
Amelie CoolkensRadiobiology Unit, Institute for Environment, Health and Safety, Belgian Nuclear Research Centre (SCK CEN), Mol 2400, Belgium.
Sarah BaatoutRadiobiology Unit, Institute for Environment, Health and Safety, Belgian Nuclear Research Centre (SCK CEN), Mol 2400, Belgium.
Lieve MoonsNeural Circuit Development and Regeneration Research Group, Department of Biology, KU Leuven, Leuven 3000, Belgium.
Mieke VerslegersRadiobiology Unit, Institute for Environment, Health and Safety, Belgian Nuclear Research Centre (SCK CEN), Mol 2400, Belgium.
Roel QuintensRadiobiology Unit, Institute for Environment, Health and Safety, Belgian Nuclear Research Centre (SCK CEN), Mol 2400, Belgium.
Belgian Nuclear Research Centre · BEKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epigenetic clocks are based on age-associated changes in DNA methylation of CpG-sites, which can accurately measure chronological age in different species. Recently, several studies have indicated that the difference between chronological and epigenetic age, defined as the age acceleration, could reflect biological age indicating functional decline and age-associated diseases. In humans, an epigenetic clock associated Alzheimer's disease (AD) pathology with an acceleration of the epigenetic age. In this study, we developed and validated two mouse brain region-specific epigenetic clocks from the C57BL/6J hippocampus and cerebral cortex. Both clocks, which could successfully estimate chronological age, were further validated in a widely used mouse model for AD, the triple transgenic AD (3xTg-AD) mouse. We observed an epigenetic age acceleration indicating an increased biological age for the 3xTg-AD mice compared to non-pathological C57BL/6J mice, which was more pronounced in the cortex as compared to the hippocampus. Genomic region enrichment analysis revealed that age-dependent CpGs were enriched in genes related to developmental, aging-related, neuronal and neurodegenerative functions. Due to the limited access of human brain tissues, these epigenetic clocks specific for mouse cortex and hippocampus might be important in further unravelling the role of epigenetic mechanisms underlying AD pathology or brain aging in general.

Indexed as

Epigenesis, GeneticAlzheimer DiseaseAnimalsBiological ClocksCerebral CortexDisease Models, AnimalDNA MethylationFemaleHippocampusMaleMiceMice, Inbred C57BLAlzheimer's diseasecortexDNA methylationepigenetic clockhippocampus

Identifiers

PMID33082299
PMCPMC7655172
OpenAlexW3093934958

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.