Evidence map›Paper›PMID 41639284›Full record

ArticleScientific reports2026

Nicotinamide counteracts Rotenone-induced mitochondrial and neuronal dysfunction in a translational early-life model.

Amanda Siena, Luiz Felipe Souza E Silva, Vitória Cristina Araujo, Martina Raissa Ribeiro, Larissa de Sá Lima, Diana Zukas Andreotti, Ana Maria Orellana, Elisa Mitiko Kawamoto, Pedro Ismael Silva Junior, Cristoforo Scavone and 1 more

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Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Amanda SienaLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Luiz Felipe Souza E SilvaLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Vitória Cristina AraujoLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Martina Raissa RibeiroLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Larissa de Sá LimaLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Diana Zukas AndreottiLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Ana Maria OrellanaLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Elisa Mitiko KawamotoLaboratory of Molecular and Functional Neurobiology, Institute of Biomedical Science, University of São Paulo, São Paulo, Brazil.
Pedro Ismael Silva JuniorLaboratory of Applied Toxinology - Butantan Institute, São Paulo, SP, Brazil.
Cristoforo ScavoneLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil. cristoforo.scavone@gmail.com.
Tatiana Rosado RosenstockLaboratory of Molecular Neuropharmacology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico 403646/2021-9Conselho Nacional de Desenvolvimento Científico e Tecnológico 472744/2012-7Coordenação de Aperfeiçoamento de Pessoal de Nível Superior 88887.125409/2016-00Fundação de Amparo à Pesquisa do Estado de São Paulo 2015/02041-1Fundação de Amparo à Pesquisa do Estado de São Paulo 2016/22996-9Fundação de Amparo à Pesquisa do Estado de São Paulo 2018/13814-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2021/03021-5Fundação de Amparo à Pesquisa do Estado de São Paulo 2021/06009-6Fundação de Amparo à Pesquisa do Estado de São Paulo 2021/12906-0Fundação de Amparo à Pesquisa do Estado de São Paulo 2023-01789-9
6 · The paper itself

Abstract

Mitochondrial function is essential for key neurodevelopmental processes, including cellular proliferation, differentiation, migration, synaptogenesis, and synaptic pruning. Previous research from our group demonstrated that neonatal administration of Rotenone (Rot), a mitochondrial complex I inhibitor, led to mitochondrial dysfunction and schizophrenia-like behavioral phenotypes. In this study, we aimed to identify possible cellular pathways disrupted by Rot exposure that may underlie these behavioral alterations. Thus, primary cortical neurons were treated with 1.325 nM Rot for 24 h, a concentration extrapolated from cortical levels observed in the neonatal Rot model. This treatment impaired mitochondrial complex I activity, decreased superoxide production, disrupted mitochondrial respiration and dynamics, reduced dendritic branching, and decreased synapse formation. Notably, pretreatment with Nicotinamide (NAM), a NAD precursor, improved mitochondrial function, reversing these effects. Altogether, our findings underscore the critical role of mitochondrial integrity in neurodevelopment and its potential contribution to neurodevelopmental disorders such as schizophrenia.

Indexed as

MitochondriaNeuronsNiacinamideRotenoneAnimalsCells, CulturedElectron Transport Complex IMitochondrial DynamicsNeurodevelopmentElectron Transport Complex INiacinamideRotenoneCell respirationDendritic spinesMitochondrial dynamicsNeurodevelopmental disordersSchizophrenia

Identifiers

PMID41639284
PMCPMC12921318

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.