Evidence map›Paper›PMID 25578949›Full record

ReviewNeuroscience letters2015

Dendritic spine dysgenesis in autism related disorders.

Mary Phillips, Lucas Pozzo-Miller

Abstract readReview
In one paragraph

Review in Neuroscience letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers.

0numbers the graph read from it
0cells of the map it votes in
111citing papers in PubMed
11.6field-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

111 citing papers in PubMed, 185 citations in OpenAlex.

  1. Article
  2. Maternal Extracellular Vesicles During Pregnancy and Autism Risk in Children.medRxiv : the preprint server for health sciences · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Altered Structural Plasticity Mediated by mGlu and NMDA Receptors and Impaired Cognition in a Genetic ASD Model (Shank3The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Autism-associatedProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Activation of GABA transmission by clonazepam reverses the autistic-like phenotypes of the Cav3.2 knockout mice.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

51 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.

Mary PhillipsDepartment of Neurobiology, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL 35294, USA.
Lucas Pozzo-MillerDepartment of Neurobiology, Civitan International Research Center, The University of Alabama at Birmingham, Birmingham, AL 35294, USA. Electronic address: lucaspm@uab.edu.
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
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 HD-074418NICHD NIH HHS R21 HD074418NINDS NIH HHS NS-065027NINDS NIH HHS R01 NS040593NINDS NIH HHS R01 NS065027
6 · The paper itself

Abstract

The activity-dependent structural and functional plasticity of dendritic spines has led to the long-standing belief that these neuronal compartments are the subcellular sites of learning and memory. Of relevance to human health, central neurons in several neuropsychiatric illnesses, including autism related disorders, have atypical numbers and morphologies of dendritic spines. These so-called dendritic spine dysgeneses found in individuals with autism related disorders are consistently replicated in experimental mouse models. Dendritic spine dysgenesis reflects the underlying synaptopathology that drives clinically relevant behavioral deficits in experimental mouse models, providing a platform for testing new therapeutic approaches. By examining molecular signaling pathways, synaptic deficits, and spine dysgenesis in experimental mouse models of autism related disorders we find strong evidence for mTOR to be a critical point of convergence and promising therapeutic target.

Indexed as

Angelman SyndromeAnimalsChild Development Disorders, PervasiveDendritic SpinesDown SyndromeFragile X SyndromeHumansIntellectual DisabilityRett SyndromeTuberous SclerosisFragile XIntellectual disabilityMeCP2mGluRmTORRett syndromeTrkB

Identifiers

PMID25578949
PMCPMC4496332
OpenAlexW2072358341

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.