Evidence map›Paper›PMID 32826066›Full record

ArticleBiological psychiatry2021

Atypical Neurogenesis in Induced Pluripotent Stem Cells From Autistic Individuals.

Dwaipayan Adhya, Vivek Swarup, Roland Nagy, Lucia Dutan, Carole Shum, Eva P Valencia-Alarcón, Kamila Maria Jozwik, Maria Andreina Mendez, Jamie Horder, Eva Loth and 11 more

Open access · hybridAbstract read
In one paragraph

Article in Biological psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

42 citing papers in PubMed, 63 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. A Review of the Effects of Maternal and Paternal Obesity on Neurodevelopmental Disorders and Related Neurobiology in Rodent and Human Offspring.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026
    Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
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  14. Article
  15. Article
  16. Using Organoids to Model Sex Differences in the Human Brain.Biological psychiatry global open science · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Pleiotropy of autism-associated chromatin regulators.Development (Cambridge, England) · 2023
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 6 institutions in 2 countries.

Dwaipayan AdhyaAutism Research Centre, Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom; Department of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Vivek SwarupProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California.
Roland NagyDepartment of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Lucia DutanDepartment of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Carole ShumDepartment of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Eva P Valencia-AlarcónDepartment of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Kamila Maria JozwikCancer Research UK Cambridge Institute, Cambridge, United Kingdom.
Maria Andreina MendezDepartment of Forensic and Neurodevelopmental Sciences, Sackler Institute for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Jamie HorderDepartment of Forensic and Neurodevelopmental Sciences, Sackler Institute for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Eva LothDepartment of Forensic and Neurodevelopmental Sciences, Sackler Institute for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Paulina NowosiadDepartment of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Irene LeeBehavioural and Brain Sciences Unit, Population Policy Practice Programme, Great Ormond Street Institute of Child Health, University College London, London, United Kingdom.
David SkuseBehavioural and Brain Sciences Unit, Population Policy Practice Programme, Great Ormond Street Institute of Child Health, University College London, London, United Kingdom.
Frances A FlinterDepartment of Clinical Genetics, Guy's and St. Thomas' NHS Foundation Trust, London, United Kingdom.
Declan MurphyDepartment of Forensic and Neurodevelopmental Sciences, Sackler Institute for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Grainne McAlonanDepartment of Forensic and Neurodevelopmental Sciences, Sackler Institute for Translational Neurodevelopment, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom.
Daniel H GeschwindProgram in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California; Department of Human Genetics, University of California, Los Angeles, Los Angeles, California.
Jack PriceDepartment of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom; MRC Centre for Neurodevelopmental Disorders, King's College London, London, United Kingdom.
Jason CarrollCancer Research UK Cambridge Institute, Cambridge, United Kingdom.
Deepak P SrivastavaDepartment of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, United Kingdom; MRC Centre for Neurodevelopmental Disorders, King's College London, London, United Kingdom. Electronic address: deepak.srivastava@kcl.ac.uk.
Simon Baron-CohenAutism Research Centre, Department of Psychiatry, University of Cambridge, Cambridge, United Kingdom.
King's College London · GBCancer Research UK Cambridge Center · GBGreat Ormond Street Hospital · GBUniversity of California, Los Angeles · USGuy's and St Thomas' NHS Foundation Trust · GBUniversity of Cambridge · GB

Funding

Medical Research Council MR/L021064/1Medical Research Council MR/N026063/1Medical Research Council MR/W006251/1Wellcome Trust
6 · The paper itself

Abstract

backgroundAutism is a heterogeneous collection of disorders with a complex molecular underpinning. Evidence from postmortem brain studies have indicated that early prenatal development may be altered in autism. Induced pluripotent stem cells (iPSCs) generated from individuals with autism with macrocephaly also indicate prenatal development as a critical period for this condition. But little is known about early altered cellular events during prenatal stages in autism.

methodsiPSCs were generated from 9 unrelated individuals with autism without macrocephaly and with heterogeneous genetic backgrounds, and 6 typically developing control individuals. iPSCs were differentiated toward either cortical or midbrain fates. Gene expression and high throughput cellular phenotyping was used to characterize iPSCs at different stages of differentiation.

resultsA subset of autism-iPSC cortical neurons were RNA-sequenced to reveal autism-specific signatures similar to postmortem brain studies, indicating a potential common biological mechanism. Autism-iPSCs differentiated toward a cortical fate displayed impairments in the ability to self-form into neural rosettes. In addition, autism-iPSCs demonstrated significant differences in rate of cell type assignment of cortical precursors and dorsal and ventral forebrain precursors. These cellular phenotypes occurred in the absence of alterations in cell proliferation during cortical differentiation, differing from previous studies. Acquisition of cell fate during midbrain differentiation was not different between control- and autism-iPSCs.

conclusionsTaken together, our data indicate that autism-iPSCs diverge from control-iPSCs at a cellular level during early stage of neurodevelopment. This suggests that unique developmental differences associated with autism may be established at early prenatal stages.

Indexed as

Autistic DisorderInduced Pluripotent Stem CellsCell DifferentiationFemaleHumansNeurogenesisNeuronsPregnancyAutismCortical differentiationFunctional genomicsMidbrain differentiationNeural precursorsNeural progenitor cellsNeurodevelopment

Identifiers

PMID32826066
PMCPMC7843956
OpenAlexW3038126759

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.