Evidence map›Paper›PMID 24006237›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2013

Acetyltransferases (HATs) as targets for neurological therapeutics.

Anne Schneider, Snehajyoti Chatterjee, Olivier Bousiges, B Ruthrotha Selvi, Amrutha Swaminathan, Raphaelle Cassel, Frédéric Blanc, Tapas K Kundu, Anne-Laurence Boutillier

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

56 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
  2. Epigenetic Targeting in Myeloid Malignancies.Advances in experimental medicine and biology · 2026
    Review
  3. Review
  4. Epigenetic alterations in Myeloid Malignancies.Advances in experimental medicine and biology · 2026
    Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  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

9 authors at 5 institutions in 2 countries.

Anne SchneiderLaboratoire de Neurosciences Cognitives et Adaptatives (LNCA), UMR7364, Université de Strasbourg-CNRS, GDR CNRS 2905, Faculté de Psychologie, 12 rue Goethe, 67000, Strasbourg, France.
Snehajyoti Chatterjee
Olivier Bousiges
B Ruthrotha Selvi
Amrutha Swaminathan
Raphaelle Cassel
Frédéric Blanc
Tapas K Kundu
Anne-Laurence Boutillier
Jawaharlal Nehru Centre for Advanced Scientific Research · INLaboratoire de Neurosciences Cognitives et Adaptatives · FRUniversité de Strasbourg · FRCentre National de la Recherche Scientifique · FRHôpital Civil, Strasbourg · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The acetylation of histone and non-histone proteins controls a great deal of cellular functions, thereby affecting the entire organism, including the brain. Acetylation modifications are mediated through histone acetyltransferases (HAT) and deacetylases (HDAC), and the balance of these enzymes regulates neuronal homeostasis, maintaining the pre-existing acetyl marks responsible for the global chromatin structure, as well as regulating specific dynamic acetyl marks that respond to changes and facilitate neurons to encode and strengthen long-term events in the brain circuitry (e.g., memory formation). Unfortunately, the dysfunction of these finely-tuned regulations might lead to pathological conditions, and the deregulation of the HAT/HDAC balance has been implicated in neurological disorders. During the last decade, research has focused on HDAC inhibitors that induce a histone hyperacetylated state to compensate acetylation deficits. The use of these inhibitors as a therapeutic option was efficient in several animal models of neurological disorders. The elaboration of new cell-permeant HAT activators opens a new era of research on acetylation regulation. Although pathological animal models have not been tested yet, HAT activator molecules have already proven to be beneficial in ameliorating brain functions associated with learning and memory, and adult neurogenesis in wild-type animals. Thus, HAT activator molecules contribute to an exciting area of research.

Indexed as

AcetylationAcetyltransferasesHistone AcetyltransferasesHistonesHumansNervous System DiseasesNeuronsAcetyltransferasesHistone AcetyltransferasesHistones

Identifiers

PMID24006237
PMCPMC3805875
OpenAlexW2029002395

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.