Evidence map›Paper›PMID 27071785›Full record

ReviewCNS & neurological disorders drug targets2016

Autism, Mitochondria and Polybrominated Diphenyl Ether Exposure.

Sarah Wong, Cecilia Giulivi

Open access · greenAbstract readReview
In one paragraph

Review in CNS & neurological disorders drug targets, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 18 citations in OpenAlex.

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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.

Sarah Wong
Cecilia GiuliviUniversity of California, Department of Molecular Biosciences, 1089 Veterinary Medicine Dr., 3009 VetMed3B, Davis, CA 95616, USA. cgiulivi@ucdavis.edu.
University of California, Davis · US

Funding

THE CHARGE STUDY: CHILDHOOD AUTISM RISKS FROM GENETICS AND THE ENVIRONMENT - ADMINISTRATIVE SUPPLEMENTR01ES015359 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HERTZ-PICCIOTTO, IRVA · 2007 to 2019
$13.8M
UC Davis Center for Children's Environmental Health (CCEH)P01ES011269 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI VAN DE WATER, JUDY A. · 2001 to 2018
$12.5M
Autism Risk, Prenatal Environmental Exposures, and Pathophysiologic MarkersR01ES020392 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HERTZ-PICCIOTTO, IRVA, OZONOFF, SALLY · 2011 to 2015
$9.0M
Environmental Influence on Infant Microbiome Development and ASD SymptomsR01ES028089 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI HERTZ-PICCIOTTO, IRVA, MILLS, DAVID ANDREW · 2016 to 2020
$3.6M
BUILDS MARBLES: Biorepository Upkeep and Infrastructure for Longitudinal Data Sharing for MARBLESR24ES028533 · NIEHS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI Brittany D. Chambers Butcher, Rebecca Jean Schmidt · 2017 to 2026
$2.3M
Influence of Prenatal Folate on Placental mtDNA and Autism RiskR21HD086769 · NICHD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI GIULIVI, CECILIA, SCHMIDT, REBECCA JEAN · 2016 to 2017
$431k
Antioxidants and oxidative damage in mitochondriaR01ES012691 · NIEHS · UNIVERSITY OF CALIFORNIA DAVIS · PI GIULIVI, CECILIA · 2004 to 2004
$148k
NICHD NIH HHS R21 HD086769NIEHS NIH HHS P01 ES011269NIEHS NIH HHS R01 ES012691NIEHS NIH HHS R01 ES015359NIEHS NIH HHS R01 ES020392NIEHS NIH HHS R01 ES028089NIEHS NIH HHS R24 ES028533
6 · The paper itself

Abstract

backgroundAutism spectrum disorders (ASD) are a growing concern with more than 1 in every 68 children affected in the United States by age 8. Limited scientific advances have been made regarding the etiology of autism, with general agreement that both genetic and environmental factors contribute to this disorder.

objectiveTo explore the link between exposure to PBDE, mitochondrial dysfunction and autism risk.

resultsPerinatal exposures to PBDEs may contribute to the etiology or morbidity of ASD including mitochondrial dysfunction based on (i) their increased environmental abundance and human exposures, (ii) their activity towards implicated in neuronal development and synaptic plasticity including mitochondria, and (iii) their bioaccumulation in mitochondria.

conclusionIn this review, we propose that PBDE, and possibly other environmental exposures, during child development can induce or compound mitochondrial dysfunction, which in conjunction with a dysregulated antioxidant response, increase a child's susceptibility of autism.

Indexed as

Environmental ExposureAutism Spectrum DisorderAutistic DisorderChildChild DevelopmentFemaleHalogenated Diphenyl EthersHumansMaleMitochondriaMitochondrial DiseasesHalogenated Diphenyl Ethers

Identifiers

PMID27071785
PMCPMC5266592
OpenAlexW2341447592

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.