Evidence map›Paper›PMID 23333625›Full record

ArticleNeurobiology of disease2013

Mitochondrial abnormalities in temporal lobe of autistic brain.

Guomei Tang, Puri Gutierrez Rios, Sheng-Han Kuo, Hasan Orhan Akman, Gorazd Rosoklija, Kurenai Tanji, Andrew Dwork, Eric A Schon, Salvatore Dimauro, James Goldman and 1 more

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 2 pooled it
8.6field-weighted citation impact, top 2% 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

100 citing papers in PubMed, 2 syntheses or guidelines pooled it, 191 citations in OpenAlex.

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  20. In vivo translocator protein in females with autism spectrum disorder: a pilot study.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article

40 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

11 authors at 1 institution in 1 country.

Guomei TangDepartment of Neurology, Columbia University, NY 10032, USA.
Puri Gutierrez Rios
Sheng-Han Kuo
Hasan Orhan Akman
Gorazd Rosoklija
Kurenai Tanji
Andrew Dwork
Eric A Schon
Salvatore Dimauro
James Goldman
David Sulzer
Columbia University · US

Funding

THERAPEUTIC APPROACHES IN MODELS OF MITOCHONDRIAL DIS.P01HD032062 · NICHD · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI DAVIDSON, MERCY MASCREEN · 1995 to 2014
$24.4M
Golgi Studies of SchizophreniaR01MH064168 · NIMH · NEW YORK STATE PSYCHIATRIC INSTITUTE DBA RESEARCH FOUNDATION FOR MENTAL HYGIENE, INC · PI DWORK, ANDREW J · 2001 to 2013
$4.3M
The role of glucocerebrosidase and chaperone_mediated autophagy in Parkinsons disK08NS083738 · NINDS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI KUO, SHENG-HAN · 2013 to 2017
$940k
Mitochondrial dysfunction due to aberrant mTOR-regulated mitophagy in autismK01MH096956 · NIMH · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI TANG, GUOMEI · 2013 to 2016
$734k
NICHD NIH HHS P01 HD032062NIMH NIH HHS K01 MH096956NIMH NIH HHS R01 MH064168NINDS NIH HHS K08 NS083738
6 · The paper itself

Abstract

Autism spectrum disorder (ASD) consists of a group of complex developmental disabilities characterized by impaired social interactions, deficits in communication and repetitive behavior. Multiple lines of evidence implicate mitochondrial dysfunction in ASD. In postmortem BA21 temporal cortex, a region that exhibits synaptic pathology in ASD, we found that compared to controls, ASD patients exhibited altered protein levels of mitochondria respiratory chain protein complexes, decreased Complex I and IV activities, decreased mitochondrial antioxidant enzyme SOD2, and greater oxidative DNA damage. Mitochondrial membrane mass was higher in ASD brain, as indicated by higher protein levels of mitochondrial membrane proteins Tom20, Tim23 and porin. No differences were observed in either mitochondrial DNA or levels of the mitochondrial gene transcription factor TFAM or cofactor PGC1α, indicating that a mechanism other than alterations in mitochondrial genome or mitochondrial biogenesis underlies these mitochondrial abnormalities. We further identified higher levels of the mitochondrial fission proteins (Fis1 and Drp1) and decreased levels of the fusion proteins (Mfn1, Mfn2 and Opa1) in ASD patients, indicating altered mitochondrial dynamics in ASD brain. Many of these changes were evident in cortical pyramidal neurons, and were observed in ASD children but were less pronounced or absent in adult patients. Together, these findings provide evidence that mitochondrial function and intracellular redox status are compromised in pyramidal neurons in ASD brain and that mitochondrial dysfunction occurs during early childhood when ASD symptoms appear.

Indexed as

AdolescentAdultAutistic DisorderBlotting, WesternChildChild, PreschoolElectron Transport Chain Complex ProteinsFemaleHumansMaleMiddle AgedMitochondriaOxidative StressTemporal LobeYoung AdultElectron Transport Chain Complex Proteins

Identifiers

PMID23333625
PMCPMC3959772
OpenAlexW2060836360

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.