Evidence map›Paper›PMID 23597512›Full record

ReviewNeuropharmacology2014

BDNF deregulation in Rett syndrome.

Wei Li, Lucas Pozzo-Miller

Abstract readReview
In one paragraph

Review in Neuropharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
11.8field-weighted citation impact, top 1% 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

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 175 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Targeted BDNF upregulation via upstream open reading frame disruption.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  6. Article
  7. Article
  8. The CaInternational journal of molecular sciences · 2025
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Disorders of puberty and neurodevelopment: A shared etiology?Annals of the New York Academy of Sciences · 2024
    Review

49 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Wei LiDepartment of Neurobiology, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Lucas Pozzo-Miller
Civitan International · US

Funding

ACTIONS OF BDNF ON CA2+ SIGNALS IN HIPPOCAMPAL NEURONSR01NS040593 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POZZO-MILLER, LUCAS D · 2000 to 2010
$2.8M
MeCP2 Modulation of BDNF Signaling: Shared Mechanisms of Rett and AutismR01NS065027 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POZZO-MILLER, LUCAS D · 2010 to 2014
$1.7M
NINDS NIH HHS NS-065027NINDS NIH HHS NS-40593NINDS NIH HHS R01 NS040593NINDS NIH HHS R01 NS065027
6 · The paper itself

Abstract

BDNF is the best-characterized neurotrophin in terms of its gene structure and modulation, secretion processing, and signaling cascades following its release. In addition to diverse features at the genetic and molecular levels, the abundant expression in several regions of the central nervous system has implicated BDNF as a potent modulator in many aspects of neuronal development, as well as synaptic transmission and plasticity. Impairments in any of these critical functions likely contribute to a wide array of neurodevelopmental, neurodegenerative, and neuropsychiatric diseases. In this review, we focus on a prevalent neurodevelopmental disorder, Rett syndrome (RTT), which afflicts 1:15,000 women world-wide. We describe the consequences of loss-of-function mutations in the gene encoding the transcription factor methyl-CpG binding protein 2 (MeCP2) in RTT, and then elaborate on the current understanding of how MeCP2 controls BDNF expression. Finally, we discuss the literature regarding alterations in BDNF levels in RTT individuals and MeCP2-based mouse models, as well as recent progress in searching for rational therapeutic interventions. This article is part of the Special Issue entitled 'BDNF Regulation of Synaptic Structure, Function, and Plasticity'.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorFemaleHumansMethyl-CpG-Binding Protein 2MiceMutationRett SyndromeBrain-Derived Neurotrophic FactorMECP2 protein, humanMethyl-CpG-Binding Protein 2BDNFIntellectual disabilityMeCP2Mouse modelsRett syndrome

Identifiers

PMID23597512
PMCPMC3773283
OpenAlexW1970151100

What OpenQuestion holds

Textmetadata
LicenceTDM
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.