Evidence map›Paper›PMID 24441681›Full record

ArticleNature neuroscience2014

Epigenetic suppression of neuroligin 1 underlies amyloid-induced memory deficiency.

Bihua Bie, Jiang Wu, Hui Yang, Jijun J Xu, David L Brown, Mohamed Naguib

Abstract read
PubMed Publisher
In one paragraph

Article in Nature neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

60 citing papers in PubMed, 101 citations in OpenAlex.

  1. Declining levels of functionally specialized synaptic proteins in plasma neuronal exosomes with progression of Alzheimer's disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Trial
  2. The histone deacetylase family in health and disease.Signal transduction and targeted therapy · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Epigenetics-targeted drugs: current paradigms and future challenges.Signal transduction and targeted therapy · 2024
    Review
  9. Article
  10. Article
  11. Synapse Regulation.Advances in neurobiology · 2024
    Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. [Nature communications · 2022
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Bihua Bie1] Department of General Anesthesiology, Anesthesiology Institute, Cleveland Clinic, Cleveland, Ohio, USA. [2].
Jiang Wu1] Department of General Anesthesiology, Anesthesiology Institute, Cleveland Clinic, Cleveland, Ohio, USA. [2].
Hui YangDepartment of General Anesthesiology, Anesthesiology Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Jijun J XuDepartment of General Anesthesiology, Anesthesiology Institute, Cleveland Clinic, Cleveland, Ohio, USA.
David L BrownDepartment of General Anesthesiology, Anesthesiology Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Mohamed NaguibDepartment of General Anesthesiology, Anesthesiology Institute, Cleveland Clinic, Cleveland, Ohio, USA.
Cleveland Clinic · US

Funding

Clinical and Translational Science Collaborative of ClevelandUL1TR000439 · NCATS · CASE WESTERN RESERVE UNIVERSITY · PI KONSTAN, MICHAEL W. · 2012 to 2016
$50.0M
NCATS NIH HHS UL1 TR000439
6 · The paper itself

Abstract

Amyloid-induced microglial activation and neuroinflammation impair central synapses and memory function, although the mechanism remains unclear. Neuroligin 1 (NLGN1), a postsynaptic protein found in central excitatory synapses, governs excitatory synaptic efficacy and plasticity in the brain. Here we found, in rodents, that amyloid fibril-induced neuroinflammation enhanced the interaction between histone deacetylase 2 and methyl-CpG-binding protein 2, leading to suppressed histone H3 acetylation and enhanced cytosine methylation in the Nlgn1 promoter region and decreased NLGN1 expression, underlying amyloid-induced memory deficiency. Manipulation of microglia-associated neuroinflammation modulated the epigenetic modification of the Nlgn1 promoter, hippocampal glutamatergic transmission and memory function. These findings link neuroinflammation, synaptic efficacy and memory, thus providing insight into the pathogenesis of amyloid-associated diseases.

Indexed as

Memory DisordersAmyloidAmyloid beta-Protein PrecursorAnimalsCell Adhesion Molecules, NeuronalDisease Models, AnimalDNA MethylationExcitatory Amino Acid AntagonistsHippocampusHistone Deacetylase 2HumansIn Vitro TechniquesLipopolysaccharidesMaleMaze LearningMembrane PotentialsAmyloidAmyloid beta-Protein PrecursorCell Adhesion Molecules, NeuronalExcitatory Amino Acid AntagonistsHdac2 protein, mouseHistone Deacetylase 2LipopolysaccharidesMethyl-CpG-Binding Protein 2neuroligin 1Presenilin-1PSEN1 protein, human

Identifiers

PMID24441681
OpenAlexW2135849687

What OpenQuestion holds

Textmetadata
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.