Evidence map›Paper›PMID 25309341›Full record

ReviewFrontiers in neuroanatomy2014

Dendritic spine dysgenesis in Rett syndrome.

Xin Xu, Eric C Miller, Lucas Pozzo-Miller

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in neuroanatomy, 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
6.5field-weighted citation impact, top 3% 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, 91 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. The CaInternational journal of molecular sciences · 2025
    Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. iScience · 2024
    Article
  16. Rett and Rett-related disorders: Common mechanisms for shared symptoms?Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  17. Review
  18. Article
  19. Article
  20. Microglia and Neurodevelopmental Disorders.Annual review of neuroscience · 2022
    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

3 authors at 2 institutions in 1 country.

Xin XuDepartment of Neurobiology, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL USA.
Eric C MillerDepartment of Neurobiology, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL USA.
Lucas Pozzo-MillerDepartment of Neurobiology, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL USA.
Civitan International · USUniversity of Alabama at Birmingham · US

Funding

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
Reversing BDNF Impairments in Rett Mice with TRPC Channel ActivatorsR21HD074418 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POZZO-MILLER, LUCAS D · 2013 to 2014
$399k
NICHD NIH HHS R21 HD074418NINDS NIH HHS R01 NS065027
6 · The paper itself

Abstract

Spines are small cytoplasmic extensions of dendrites that form the postsynaptic compartment of the majority of excitatory synapses in the mammalian brain. Alterations in the numerical density, size, and shape of dendritic spines have been correlated with neuronal dysfunction in several neurological and neurodevelopmental disorders associated with intellectual disability, including Rett syndrome (RTT). RTT is a progressive neurodevelopmental disorder associated with intellectual disability that is caused by loss of function mutations in the transcriptional regulator methyl CpG-binding protein 2 (MECP2). Here, we review the evidence demonstrating that principal neurons in RTT individuals and Mecp2-based experimental models exhibit alterations in the number and morphology of dendritic spines. We also discuss the exciting possibility that signaling pathways downstream of brain-derived neurotrophic factor (BDNF), which is transcriptionally regulated by MeCP2, offer promising therapeutic options for modulating dendritic spine development and plasticity in RTT and other MECP2-associated neurodevelopmental disorders.

Indexed as

autism spectrum disorderBDNFexcitatory synapsehippocampusMeCP2organotypic slice culturesspine densityTrkB

Identifiers

PMID25309341
PMCPMC4159975
OpenAlexW2050954502

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.