Evidence map›Paper›PMID 33823515›Full record

ReviewDevelopmental neuroscience2021

Abnormal Cerebellar Development in Autism Spectrum Disorders.

Meike E van der Heijden, Jason S Gill, Roy V Sillitoe

Open access · greenAbstract 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 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
8.6field-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

62 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Review
  3. Early autism risk factors: a cohort study of children born very preterm at 5-years.Journal of perinatology : official journal of the California Perinatal Association · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
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  10. Article
  11. Brain-wide mapping of developmental trajectories of cerebellar efferent projections.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  12. Cell-type-resolvedbioRxiv : the preprint server for biology · 2025
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Article

2 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

3 authors at 1 institution in 1 country.

Meike E van der HeijdenDepartment of Pathology & Immunology, Baylor College of Medicine, Houston, Texas, USA.
Jason S GillJan and Dan Duncan Neurological Research Institute at Texas Children's Hospital, Houston, Texas, USA.
Roy V SillitoeDepartment of Pathology & Immunology, Baylor College of Medicine, Houston, Texas, USA.
Baylor College of Medicine · US

Funding

Preclinical and Clincial OutcomesP50HD103555 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI Sandesh Chakravarthy Sreenath Nagamani, David Loren Nelson · 2020 to 2026
$9.9M
Cerebellar Deep Brain StimulationR01NS119301 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI SILLITOE, ROY VINCENT · 2020 to 2024
$2.0M
CEREBELLAR FUNCTION IN TREMORR01NS100874 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI SILLITOE, ROY VINCENT · 2017 to 2021
$1.9M
SYNAPTIC ORIGINS OF CEREBELLAR DISEASER01NS089664 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI SILLITOE, ROY VINCENT · 2014 to 2018
$1.7M
NICHD NIH HHS P50 HD103555NINDS NIH HHS R01 NS089664NINDS NIH HHS R01 NS100874NINDS NIH HHS R01 NS119301
6 · The paper itself

Abstract

Autism spectrum disorders (ASD) comprise a group of heterogeneous neurodevelopmental conditions characterized by impaired social interactions and repetitive behaviors with symptom onset in early infancy. The genetic risks for ASD have long been appreciated: concordance of ASD diagnosis may be as high as 90% for monozygotic twins and 30% for dizygotic twins, and hundreds of mutations in single genes have been associated with ASD. Nevertheless, only 5-30% of ASD cases can be explained by a known genetic cause, suggesting that genetics is not the only factor at play. More recently, several studies reported that up to 40% of infants with cerebellar hemorrhages and lesions are diagnosed with ASD. These hemorrhages are overrepresented in severely premature infants, who are born during a period of highly dynamic cerebellar development that encompasses an approximately 5-fold size expansion, an increase in structural complexity, and remarkable rearrangements of local neural circuits. The incidence of ASD-causing cerebellar hemorrhages during this window supports the hypothesis that abnormal cerebellar development may be a primary risk factor for ASD. However, the links between developmental deficits in the cerebellum and the neurological dysfunctions underlying ASD are not completely understood. Here, we discuss key processes in cerebellar development, what happens to the cerebellar circuit when development is interrupted, and how impaired cerebellar function leads to social and cognitive impairments. We explore a central question: Is cerebellar development important for the generation of the social and cognitive brain or is the cerebellum part of the social and cognitive brain itself?

Indexed as

Autism Spectrum DisorderBrainCerebellumHumansInfantAutism spectrum disordersCerebellumCognitionConnectivityMorphogenesisSocial behavior

Identifiers

PMID33823515
PMCPMC8440334
OpenAlexW3152448303

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.