Evidence map›Paper›PMID 27628303›Full record

ReviewCellular and molecular life sciences : CMLS2017

Epigenetic dysregulation of brainstem nuclei in the pathogenesis of Alzheimer's disease: looking in the correct place at the right time?

A Iatrou, G Kenis, B P F Rutten, K Lunnon, D L A van den Hove

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Genome-wide methylomic regulation of multiscale gene networks in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article
  5. The Mammalian Family of Katanin Microtubule-Severing Enzymes.Frontiers in cell and developmental biology · 2021
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. 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

5 authors at 3 institutions in 3 countries.

A IatrouDepartment of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Maastricht University, Universiteitssingel 50, 6200 MD, Maastricht, The Netherlands.
G KenisDepartment of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Maastricht University, Universiteitssingel 50, 6200 MD, Maastricht, The Netherlands.
B P F RuttenDepartment of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Maastricht University, Universiteitssingel 50, 6200 MD, Maastricht, The Netherlands.
K LunnonUniversity of Exeter Medical School, RILD, University of Exeter, Barrack Road, Devon, UK.
D L A van den HoveDepartment of Psychiatry and Neuropsychology, School for Mental Health and Neuroscience (MHeNS), Maastricht University, Universiteitssingel 50, 6200 MD, Maastricht, The Netherlands. d.vandenhove@maastrichtuniversity.nl.
Maastricht University · NLUniversity of Exeter · GBUniversity of Würzburg · DE

Funding

Medical Research Council MR/N027973/1
6 · The paper itself

Abstract

Even though the etiology of Alzheimer's disease (AD) remains unknown, it is suggested that an interplay among genetic, epigenetic and environmental factors is involved. An increasing body of evidence pinpoints that dysregulation in the epigenetic machinery plays a role in AD. Recent developments in genomic technologies have allowed for high throughput interrogation of the epigenome, and epigenome-wide association studies have already identified unique epigenetic signatures for AD in the cortex. Considerable evidence suggests that early dysregulation in the brainstem, more specifically in the raphe nuclei and the locus coeruleus, accounts for the most incipient, non-cognitive symptomatology, indicating a potential causal relationship with the pathogenesis of AD. Here we review the advancements in epigenomic technologies and their application to the AD research field, particularly with relevance to the brainstem. In this respect, we propose the assessment of epigenetic signatures in the brainstem as the cornerstone of interrogating causality in AD. Understanding how epigenetic dysregulation in the brainstem contributes to AD susceptibility could be of pivotal importance for understanding the etiology of the disease and for the development of novel diagnostic and therapeutic strategies.

Indexed as

DNA MethylationEpigenesis, GeneticAlzheimer DiseaseAnimalsBrain StemDorsal Raphe NucleusHumansAlzheimer’s diseaseDNA hydroxymethylationDNA methylationEpigeneticsLocus coeruleusRaphe nuclei

Identifiers

PMID27628303
PMCPMC5241349
OpenAlexW2519899359

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.