Evidence map›Paper›PMID 27547454›Full record

ReviewNeural plasticity2016

Where Environment Meets Cognition: A Focus on Two Developmental Intellectual Disability Disorders.

I De Toma, L Manubens-Gil, S Ossowski, M Dierssen

Open access · goldAbstract readReview
In one paragraph

Review in Neural plasticity, 2016. 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
1.5field-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, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Behavioral Phenotyping for Down Syndrome in Mice.Current protocols in mouse biology · 2020
    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

4 authors at 1 institution in 1 country.

I De TomaCellular and Systems Neurobiology, Systems Biology Program, Centre for Genomic Regulation, The Barcelona Institute of Science and Technology, 08003 Barcelona, Spain; Pompeu Fabra University, 08003 Barcelona, Spain.ORCID 0000-0003-4128-2561
L Manubens-GilCellular and Systems Neurobiology, Systems Biology Program, Centre for Genomic Regulation, The Barcelona Institute of Science and Technology, 08003 Barcelona, Spain; Pompeu Fabra University, 08003 Barcelona, Spain.ORCID 0000-0003-2036-2204
S OssowskiPompeu Fabra University, 08003 Barcelona, Spain; Genomic and Epigenomic Variation in Disease Group, Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, 08003 Barcelona, Spain.
M DierssenCellular and Systems Neurobiology, Systems Biology Program, Centre for Genomic Regulation, The Barcelona Institute of Science and Technology, 08003 Barcelona, Spain; Pompeu Fabra University, 08003 Barcelona, Spain.ORCID 0000-0003-0853-6865
Universitat Pompeu Fabra · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the most challenging questions in neuroscience is to dissect how learning and memory, the foundational pillars of cognition, are grounded in stable, yet plastic, gene expression states. All known epigenetic mechanisms such as DNA methylation and hydroxymethylation, histone modifications, chromatin remodelling, and noncoding RNAs regulate brain gene expression, both during neurodevelopment and in the adult brain in processes related to cognition. On the other hand, alterations in the various components of the epigenetic machinery have been linked to well-known causes of intellectual disability disorders (IDDs). Two examples are Down Syndrome (DS) and Fragile X Syndrome (FXS), where global and local epigenetic alterations lead to impairments in synaptic plasticity, memory, and learning. Since epigenetic modifications are reversible, it is theoretically possible to use epigenetic drugs as cognitive enhancers for the treatment of IDDs. Epigenetic treatments act in a context specific manner, targeting different regions based on cell and state specific chromatin accessibility, facilitating the establishment of the lost balance. Here, we discuss epigenetic studies of IDDs, focusing on DS and FXS, and the use of epidrugs in combinatorial therapies for IDDs.

Indexed as

Gene-Environment InteractionAntioxidantsCatechinCognitionDNA MethylationDown SyndromeEpigenesis, GeneticFragile X SyndromeGenetic TherapyHumansIntellectual DisabilityProtein Interaction Domains and MotifsAntioxidantsCatechinepigallocatechin gallate

Identifiers

PMID27547454
PMCPMC4980517
OpenAlexW2481929555

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.