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Peer-reviewedCC BYRedox Biology

Cellular redox status is linked to olfactory alterations in cognitive decline

  • Riikka Lampinen1
  • Alexey M. Afonin1
  • Laura Mussalo1
  • Simone Avesani2
  • Tana Zavodna3
  • Emily Feneberg4
  • Zdenek Krejcik3
  • Jan Topinka3
  • Sweelin Chew1
  • Heikki Löppönen5
  • Tarja Malm1
  • Rosalba Giugno2
4 more authors
  • Anthony R. White6
  • Anne M. Koivisto7
  • Elina Penttilä5
  • Katja M. Kanninen8
8 affiliations
  1. 1A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Neulaniementie 2, Kuopio, 70210, Finland
  2. 2Department of Computer Science, University of Verona, Strada le Grazie 15, Verona, 37134, Italy
  3. 3Department of Toxicology and Molecular Epidemiology, Institute of Experimental Medicine of the Czech Academy of Sciences, Videnska 1083, Prague, 142 20, Czech Republic
  4. 4Department of Neurology, Klinikum Rechts der Isar of the Technical University of Munich, Ismaninger Strasse 22, Munich, 81675, Germany
  5. 5Department of Otorhinolaryngology, University of Eastern Finland and Kuopio University Hospital, Kuopio, 70210, Finland
  6. 6Brain and Mental Health Program, QIMR Berghofer Medical Research Institute, Herston, Queensland, 4006, Australia
  7. 7NeuroCentre, Kuopio University Hospital, Kuopio, 70210, Finland; Department of Geriatrics, Helsinki University Hospital, Haartmaninkatu 8, Helsinki, 00014, Finland; Department of Neurosciences, Faculty of Medicine, University of Helsinki, Haartmaninkatu 4, Helsinki, 00014, Finland
  8. 8A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, Neulaniementie 2, Kuopio, 70210, Finland; Corresponding author.
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Abstract

Growing evidence demonstrates that olfactory dysfunction and disease-related pathology in the olfactory areas occur early in Alzheimer's disease (AD), which is the most common neurodegenerative disorder. Oxidative stress is strongly linked to AD-associated changes in the brain, yet very little is known about redox homeostasis in the peripheral olfactory tissues, and its link to olfactory dysfunction associated with early AD. The olfactory mucosa (OM), located at the rooftop of the nasal cavity is the primary organ for olfaction through odorant detection and transmission of these signals to the brain via the olfactory nerves. This study collected patient-derived biopsies of the OM from cognitively healthy donors, individuals with mild cognitive impairment (MCI) and AD. Shotgun proteomics of the biopsies provided new insights into the molecular mechanisms associated with early AD and olfactory dysfunction, which was assessed by odor identification testing. Furthermore, microRNA sequencing and quantitative analyses of electron carriers, cofactors and glutathione from the biopsy-derived primary cells of the OM were used to link these findings to cellular redox status. The results revealed mitochondrial changes and alterations to cellular defense against oxidative stress, specifically the potentially dampened NRF2 pathway, in MCI and AD OM, which were linked to impairments in odor identification. Understanding the early cellular and molecular changes occurring in the olfactory system and olfaction could aid in the early identification of individuals at risk of developing AD and pathophysiological changes of the OM in AD.

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Cite

BibTeXRIS
BibTeX
@article{lampinen2026cellular,
  title = {{Cellular redox status is linked to olfactory alterations in cognitive decline}},
  author = {Riikka Lampinen and Alexey M. Afonin and Laura Mussalo and Simone Avesani and Tana Zavodna and Emily Feneberg and Zdenek Krejcik and Jan Topinka and Sweelin Chew and Heikki Löppönen and Tarja Malm and Rosalba Giugno and Anthony R. White and Anne M. Koivisto and Elina Penttilä and Katja M. Kanninen},
  journal = {Redox Biology},
  year = {2026},
  month = oct,
  doi = {10.1016/j.redox.2026.104393},
  url = {https://doi.org/10.1016/j.redox.2026.104393},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Cellular redox status is linked to olfactory alterations in cognitive decline
AU  - Riikka Lampinen
AU  - Alexey M. Afonin
AU  - Laura Mussalo
AU  - Simone Avesani
AU  - Tana Zavodna
AU  - Emily Feneberg
AU  - Zdenek Krejcik
AU  - Jan Topinka
AU  - Sweelin Chew
AU  - Heikki Löppönen
AU  - Tarja Malm
AU  - Rosalba Giugno
AU  - Anthony R. White
AU  - Anne M. Koivisto
AU  - Elina Penttilä
AU  - Katja M. Kanninen
PY  - 2026
DA  - 2026/10/30
JO  - Redox Biology
DO  - 10.1016/j.redox.2026.104393
UR  - https://doi.org/10.1016/j.redox.2026.104393
AB  - Growing evidence demonstrates that olfactory dysfunction and disease-related pathology in the olfactory areas occur early in Alzheimer's disease (AD), which is the most common neurodegenerative disorder. Oxidative stress is strongly linked to AD-associated changes in the brain, yet very little is known about redox homeostasis in the peripheral olfactory tissues, and its link to olfactory dysfunction associated with early AD. The olfactory mucosa (OM), located at the rooftop of the nasal cavity is the primary organ for olfaction through odorant detection and transmission of these signals to the brain via the olfactory nerves. This study collected patient-derived biopsies of the OM from cognitively healthy donors, individuals with mild cognitive impairment (MCI) and AD. Shotgun proteomics of the biopsies provided new insights into the molecular mechanisms associated with early AD and olfactory dysfunction, which was assessed by odor identification testing. Furthermore, microRNA sequencing and quantitative analyses of electron carriers, cofactors and glutathione from the biopsy-derived primary cells of the OM were used to link these findings to cellular redox status. The results revealed mitochondrial changes and alterations to cellular defense against oxidative stress, specifically the potentially dampened NRF2 pathway, in MCI and AD OM, which were linked to impairments in odor identification. Understanding the early cellular and molecular changes occurring in the olfactory system and olfaction could aid in the early identification of individuals at risk of developing AD and pathophysiological changes of the OM in AD.
SN  - 2213-2317
ER  -