Evidence map›Paper›PMID 28937691›Full record

ReviewMolecular psychiatry2017

Toward a conceptual framework for early brain and behavior development in autism.

J Piven, J T Elison, M J Zylka

Erratum issuedAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 97 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed, 3 pooled it
–field-weighted citation impact
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

97 citing papers in PubMed, 3 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Social communication development in a contingent world: insights from autism.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. The Ambiguous Role of Growth Factors in Autism: What Do We Really Know?International journal of molecular sciences · 2025
    Review
  18. Article
  19. Article
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors.

J PivenCarolina Institute for Developmental Disabilities, The University of North Carolina, Chapel Hill, NC, USA.
J T ElisonInstitute of Child Development and Department of Pediatrics, University of Minnesota, Minneapolis, MN, USA.
M J ZylkaCarolina Institute for Developmental Disabilities, The University of North Carolina, Chapel Hill, NC, USA.

Funding

Cellular and molecular mechanisms governing cortical surface area overgrowth in iPSC-derived neural cells from longitudinally characterized individuals with autismR01HD055741 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Joseph Piven · 2007 to 2026
$52.6M
UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Stephanie Engel · 2001 to 2026
$36.3M
The Elongation Hypothesis of AutismDP1ES024088 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI ZYLKA, MARK J. · 2013 to 2017
$3.8M
Infant Brain and Behavioral Signatures of Later Emerging Risk for PsychopathologyR01MH104324 · NIMH · UNIVERSITY OF MINNESOTA · PI ELISON, JED THOMAS · 2014 to 2018
$2.6M
NICHD NIH HHS R01 HD055741NIEHS NIH HHS DP1 ES024088NIEHS NIH HHS P30 ES010126NIMH NIH HHS R01 MH104324
6 · The paper itself

Abstract

Studies of infant siblings of older autistic probands, who are at elevated risk for autism, have demonstrated that the defining features of autism are not present in the first year of life but emerge late in the first and into the second year. A recent longitudinal neuroimaging study of high-risk siblings revealed a specific pattern of brain development in infants later diagnosed with autism, characterized by cortical surface area hyper-expansion in the first year followed by brain volume overgrowth in the second year that is associated with the emergence of autistic social deficits. Together with new observations from genetically defined autism risk alleles and rodent model, these findings suggest a conceptual framework for the early, post-natal development of autism. This framework postulates that an increase in the proliferation of neural progenitor cells and hyper-expansion of cortical surface area in the first year, occurring during a pre-symptomatic period characterized by disrupted sensorimotor and attentional experience, leads to altered experience-dependent neuronal development and decreased elimination of neuronal processes. This process is linked to brain volume overgrowth and disruption of the refinement of neural circuit connections and is associated with the emergence of autistic social deficits in the second year of life. A better understanding of the timing of developmental brain and behavior mechanisms in autism during infancy, a period which precedes the emergence of the defining features of this disorder, will likely have important implications for designing rational approaches to early intervention.

Indexed as

Age FactorsAnimalsAttentionAutistic DisorderBrainDevelopmental DisabilitiesHumansInfantLongitudinal StudiesNeuroimagingSiblingsSocial Behavior

Identifiers

PMID28937691
PMCPMC5621737

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.