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Transcriptomic Insights into Late-Life Depression and the Role of Environmental Drinking Water Composition: A Study on 18-Month-Old Mice

  • João Pedro Costa-Nunes
  • , Kseniia Sitdikova
  • , Evgeniy Svirin
  • , Johannes de Munter
  • , Gabor Somlyai
  • , Anna Gorlova
  • , Alexandr Litavrin
  • , Gohar M. Arajyan
  • , Zlata Nefedova
  • , Alexei Lyundup
  • , Sergey Morozov
  • , Aleksei Umriukhin
  • , Sofia Iliynskaya
  • , Anton Chernopiatko
  • , Tatyana Strekalova*
  • *Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

The study of molecular mechanisms underlying late-life depression (LLD) is increasingly important in light of population aging. To date, LLD-related molecular brain changes remain poorly understood. Furthermore, environmental factors such as climate change and geography contribute to LDD risks. One overlooked factor might be deuterium—a stable hydrogen isotope—whose concentration in drinking water can vary geographically (~90–155 ppm) and alter the incidence of mood disorders. Conversely, potential effects of natural variations in deuterium content in drinking water on LLD symptoms and brain gene expression remain unknown. We conducted Illumina gene expression profiling in the hippocampi and prefrontal cortexes of 18-month-old C57BL/6J mice, a model of LLD-like behaviors, compared to 3-month-old controls. Separately, aged mice were allowed to consume deuterium-depleted (DDW, ~90 ppm) or control (~140 ppm) water for 21 days and were studied for LLD-like behaviors and Illumina gene expression of the brain. Naïve old mice displayed =2-fold significant changes of 35 genes. Housing on DDW increased their hedonic sensitivity and novelty exploration, reduced helplessness, improved memory, and significantly altered brain expression of Egr1, Per2, Homer1, Gadd45a, and Prdx4, among others. These genes revealed significant alterations in several GO-BP and KEGG pathways implicated in inflammation, cellular stress, synaptic plasticity, emotionality, and regeneration. Additionally, we found that incubation of primary neuronal cultures in DDW-containing buffer ameliorated Ca2+ influx and mitochondrial potential in a toxicity model, suggesting the involvement of mitochondrial mechanisms in the effects of decreased deuterium levels. Thus, aging induced profound brain molecular changes that may at least in part contribute to LLD pathophysiology. Reduced deuterium intake exerted modest but significant effects on LLD-related behaviors in aged mice, which can be attributed to, but not limited by ameliorated mitochondrial function and changes in brain gene expression.
Original languageEnglish
Article number10626
JournalInternational Journal of Molecular Sciences
Volume26
Issue number21
DOIs
Publication statusPublished - 1 Nov 2025

Keywords

  • aging
  • anhedonia
  • animal models
  • depression
  • deuterium
  • environment
  • Illumina gene profiling
  • late-life depression
  • mice

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