Evidence map›Paper›PMID 27050514›Full record

ArticleCell reports2016

Differential Mitochondrial Requirements for Radially and Non-radially Migrating Cortical Neurons: Implications for Mitochondrial Disorders.

Erika G Lin-Hendel, Meagan J McManus, Douglas C Wallace, Stewart A Anderson, Jeffrey A Golden

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

35 citing papers in PubMed, 85 citations in OpenAlex.

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  11. Maternal Inflammation During Pregnancy and Offspring Brain Development: The Role of Mitochondria.Biological psychiatry. Cognitive neuroscience and neuroimaging · 2022
    Review
  12. Mitochondrial and Neuronal Dysfunctions in L1 Mutant Mice.International journal of molecular sciences · 2022
    Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. An mtDNA mutant mouse demonstrates that mitochondrial deficiency can result in autism endophenotypes.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  18. Review
  19. Article
  20. Article
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

5 authors at 3 institutions in 1 country.

Erika G Lin-HendelSchool of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Developmental, Regenerative and Stem Cell Biology, Biomedical Graduate Group, University of Pennsylvania, Philadelphia, PA 19104, USA.
Meagan J McManusCenter for Mitochondrial and Epigenomic Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Douglas C WallaceCenter for Mitochondrial and Epigenomic Medicine, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA; Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Stewart A AndersonDepartment of Psychiatry, Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA. Electronic address: sande@mail.med.upenn.edu.
Jeffrey A GoldenDepartment of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. Electronic address: jagolden@partners.org.
University of Pennsylvania · USChildren's Hospital of Philadelphia · USHarvard University · US

Funding

MITOCHONDRIAL INBORN ERRORS OF METABOLISMR01NS021328 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI WALLACE, DOUGLAS C · 1985 to 2017
$6.5M
Mouse models for mitochondrial disorders caused by mutations in mtDNAR01OD010944 · OD · UNIVERSITY OF SOUTH ALABAMA · PI ALEXEYEV, MIKHAIL F., WALLACE, DOUGLAS C · 2012 to 2020
$2.6M
ANT Defects in Neurodegenerative DiseasesR01NS041850 · NINDS · UNIVERSITY OF CALIFORNIA IRVINE · PI WALLACE, DOUGLAS C · 2001 to 2005
$1.4M
A Mitochondrial Etiology of AutismR01NS070298 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI WALLACE, DOUGLAS C · 2009 to 2010
$1.3M
NIH HHS R01 OD010944NINDS NIH HHS NS070298NINDS NIH HHS NS21328NINDS NIH HHS NS41850NINDS NIH HHS NS46166NINDS NIH HHS R01 NS021328NINDS NIH HHS R01 NS041850NINDS NIH HHS R01 NS070298
6 · The paper itself

Abstract

Mitochondrial dysfunction has been increasingly linked to neurodevelopmental disorders such as intellectual disability, childhood epilepsy, and autism spectrum disorder, conditions also associated with cortical GABAergic interneuron dysfunction. Although interneurons have some of the highest metabolic demands in the postnatal brain, the importance of mitochondria during interneuron development is unknown. We find that interneuron migration from the basal forebrain to the neocortex is highly sensitive to perturbations in oxidative phosphorylation. Both pharmacologic and genetic inhibition of adenine nucleotide transferase 1 (Ant1) disrupts the non-radial migration of interneurons, but not the radial migration of cortical projection neurons. The selective dependence of cortical interneuron migration on oxidative phosphorylation may be a mechanistic pathway upon which multiple developmental and metabolic pathologies converge.

Indexed as

Cell MovementAdenine Nucleotide Translocator 1AnimalsCentrosomeCerebral CortexEmbryo, MammalianFemaleInterneuronsMaleMice, Inbred C57BLMitochondriaMitochondrial DiseasesMutationNeuronsOxidative PhosphorylationAdenine Nucleotide Translocator 1

Identifiers

PMID27050514
PMCPMC5412722
OpenAlexW2329561586

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.