Evidence map›Paper›PMID 34139699›Full record

ReviewDevelopmental neuroscience2021

Dendritic Integration Dysfunction in Neurodevelopmental Disorders.

Andrew D Nelson, Kevin J Bender

Open access · bronzeAbstract readReview
In one paragraph

Review in Developmental neuroscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
8.1field-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

17 citing papers in PubMed, 54 citations in OpenAlex.

  1. Review
  2. The Neuroimmunology of Autism.Molecular neurobiology · 2025
    Review
  3. Autism-associatedProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Cytokine Dynamics in Autism: Analysis of BMAC Therapy Outcomes.International journal of molecular sciences · 2023
    Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. 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

2 authors at 1 institution in 1 country.

Andrew D NelsonDepartment of Neurology, University of California, San Francisco, San Francisco, California, USA.
Kevin J BenderDepartment of Neurology, University of California, San Francisco, San Francisco, California, USA.
University of California, San Francisco · US

Funding

Research Programming ModuleP30EY007551 · NEI · UNIVERSITY OF HOUSTON · PI VALLABH E DAS · 1988 to 2026
$16.4M
Molecular and circuit mechanisms of antipsychoticsR01MH112729 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BENDER, KEVIN J, WHISTLER, JENNIFER L · 2017 to 2021
$2.6M
The function of SCN2A in neocortexR01MH125978 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BENDER, KEVIN J · 2021 to 2025
$2.0M
Cellular Mechanisms of Convergence Among Autism Spectrum Disorder GenesF32MH125536 · NIMH · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NELSON, ANDREW D · 2021 to 2023
$153k
NIMH NIH HHS F32 MH125536NIMH NIH HHS R01 MH112729NIMH NIH HHS R01 MH125978
6 · The paper itself

Abstract

Neurodevelopmental disorders (NDDs) that affect cognition, social interaction, and learning, including autism spectrum disorder (ASD) and intellectual disability (ID), have a strong genetic component. Our current understanding of risk genes highlights two main groups of dysfunction: those in genes that act as chromatin modifiers and those in genes that encode for proteins localized at or near synapses. Understanding how dysfunction in these genes contributes to phenotypes observed in ASD and ID remains a major question in neuroscience. In this review, we highlight emerging evidence suggesting that dysfunction in dendrites - regions of neurons that receive synaptic input - may be key to understanding features of neuronal processing affected in these disorders. Dendritic integration plays a fundamental role in sensory processing, cognition, and conscious perception, processes hypothesized to be impaired in NDDs. Many high-confidence ASD genes function within dendrites where they control synaptic integration and dendritic excitability. Further, increasing evidence demonstrates that several ASD/ID genes, including chromatin modifiers and transcription factors, regulate the expression or scaffolding of dendritic ion channels, receptors, and synaptic proteins. Therefore, we discuss how dysfunction of subsets of NDD-associated genes in dendrites leads to defects in dendritic integration and excitability and may be one core phenotype in ASD and ID.

Indexed as

Autism Spectrum DisorderIntellectual DisabilityNeurodevelopmental DisordersHumansNeuronsSynapsesAutism spectrum disorderChannelopathyDendriteEpilepsyNeurodevelopmental disorder

Identifiers

PMID34139699
PMCPMC8440332
OpenAlexW3166617098

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.