Evidence map›Paper›PMID 34279772›Full record

ArticleMolecular neurobiology2021

Dysfunction in Mitochondrial Electron Transport Chain Complex I, Pyruvate Dehydrogenase Activity, and Mutations in ND1 and ND4 Gene in Autism Spectrum Disorder Subjects from Tamil Nadu Population, India.

Iyer Mahalaxmi, Mohana Devi Subramaniam, Abilash Valsala Gopalakrishnan, Balachandar Vellingiri

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

16 citing papers in PubMed, 32 citations in OpenAlex.

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  6. Assessment of tRNAJournal of molecular neuroscience : MN · 2023
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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

4 authors at 3 institutions in 1 country.

Iyer MahalaxmiLivestock Farming and Bioresource Technology, Tamil Nadu, India.
Mohana Devi SubramaniamSN ONGC, Department of Genetics and Molecular Biology, Vision Research Foundation, Chennai, 600-006, India.
Abilash Valsala GopalakrishnanDepartment of Biomedical Sciences, School of Biosciences and Technology, Vellore Institute of Technology, Tamil Nadu, Vellore, 632 014, India.
Balachandar VellingiriHuman Molecular Cytogenetics and Stem Cell Laboratory, Department of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore, 641-046, Tamil Nadu, India. geneticbala@buc.edu.in.ORCID http://orcid.org/0000-0002-3043-6839
Bharathiar University · INOil and Natural Gas Corporation (India) · INVellore Institute of Technology University · IN

Funding

Science and Engineering Research Board ECR/2016/001688
6 · The paper itself

Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterised by impaired social interaction and behavioural abnormalities. Growing evidence proved that impairment in mitochondrial functions could inhibit energy production and may contribute to the onset of ASD. Genetic variants in the genes of mitochondrial DNA (mtDNA) could interrupt the normal energy metabolism and production in the brain which lead to a wide range of structural and functional changes in the brain resulting in ASD. The present study aims to compare the activities of mitochondrial electron transport chain (ETC) complex I, pyruvate dehydrogenase (PDH) and specific mitochondrial DNA gene (MT-ND1 and MT-ND4) variants associated with ASD subjects in the Tamil Nadu population. Mutational analysis revealed that most mutations in ASD subjects showed synonymous type followed by missense in both the ND1 and ND4 genes. Interestingly, we found that the complex I and PDH dysfunctions may have a role in ASD compared to the controls (p ≤ 0.0001). Hence, the results of the present study suggest that mitochondrial dysfunction, specifically the complex I genes, may play a major role in the onset of ASD, concluding that further research on mitochondrial genes are mandatory to unravel the mechanism behind ASD pathogenesis.

Indexed as

AdolescentAutism Spectrum DisorderChildChild, PreschoolDNA, MitochondrialElectron Transport Complex IEnzyme ActivationFemaleHumansIndiaMaleMutationNADH DehydrogenasePolymorphism, Single NucleotidePopulation SurveillancePyruvate Dehydrogenase ComplexDNA, MitochondrialElectron Transport Complex INADH DehydrogenaseNADH dehydrogenase subunit 1, humanNADH dehydrogenase subunit 4Pyruvate Dehydrogenase ComplexAutism spectrum disorderComplex I activityMitochondrial dysfunctionmtDNA gene mutationsPDH activitySingle-nucleotide polymorphism

Identifiers

PMID34279772
OpenAlexW3184823849

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.