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16 November 2025

Altered Co-Expression Patterns of Mitochondrial NADH-Dehydrogenase Genes in the Prefrontal Cortex of Rodent ADHD Models

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1
Institute of Translational Biomedicine, St. Petersburg State University, Universitetskaya Nab. 7/9, 199034 St. Petersburg, Russia
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Center for Transgenesis and Genome Editing, St. Petersburg State University, Universitetskaya Nab. 7/9, 199034 St. Petersburg, Russia
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci.2025, 26(22), 11079;https://doi.org/10.3390/ijms262211079 
(registering DOI)
This article belongs to the Special Issue New Insights in Translational Bioinformatics: Second Edition

Abstract

Altered mitochondrial function is implicated in disorders characterized by prefrontal cortex activation deficits, including attention deficit hyperactivity disorder (ADHD). The expression of mitochondrial DNA-coded respiratory chain complex I genes (ND1–ND6) in the prefrontal cortex of ADHD animal models was estimated in the present study. ND gene expression was assessed in two publicly available datasets: GSE117357 (Adgrl3 knockout mice) and GSE173926 (MYT1L heterozygous knockout mice). Additionally, we measured NDs gene expression via qPCR in dopamine transporter knockout (DAT-KO) rats and their heterozygous (DAT-Het) littermates. Transcriptomic analysis revealed consistent ND1–ND6 expression profiles across both datasets, and co-expression among ND genes was significantly enhanced in ADHD models compared to wild-type controls. Whole-transcriptome analysis identified associations between ND3 and ND4L expression and genes involved in neural tissue-specific processes, exclusively in ADHD models. In DAT-KO and DAT-Het rats, NDs gene co-expression increased. Furthermore, in DAT-Het rats, which do not exhibit hyperactivity, the upregulation of ND4L expression relative to wild-type littermates was demonstrated. The observed changes in mitochondrial complex I gene co-expression in ADHD models suggest mitochondria may serve as a prospective target for adjuvant therapy. These findings highlight the need for further investigation into mitochondrial contributions to ADHD pathophysiology.

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