{
  "abstract": "Mitochondrial dysfunction contributes to Alzheimer’s disease (AD), but the roles of individual respiratory-chain proteins remain incompletely understood. We examined mitochondrially encoded cytochrome c oxidase subunit II (MT-CO2) and nuclear encoded succinate dehydrogenase complex iron-sulfur subunit B (SDHB) in postmortem temporal cortex from cognitively normal (CN) individuals and patients with AD, Lewy body dementia/Parkinson’s disease (LBD/PD), or progressive supranuclear palsy (PSP). MT-CO2 abundance was lower in AD than in CN and LBD/PD, whereas SDHB was lower in AD than in CN, LBD/PD, and PSP. A significant protein × diagnosis interaction indicated distinct diagnostic-group patterns for MT-CO2 and SDHB. In BE(2)-C neuroblastoma cells, repeated 650 nm red-light and 808 nm near-infrared (NIR) photobiomodulation increased MT-CO2 abundance, with the largest responses following 10- and 15-min exposures. shRNA-mediated MT-CO2 reduction impaired Complex IV-dependent respiration and attenuated the bioenergetic response to 808 nm treatment. Photobiomodulation did not significantly alter mitochondrially encoded MT-CO1 or MT-CO3 abundance. These findings identify alterations in MT-CO2 and SDHB in AD temporal cortex and demonstrate that MT-CO2 contributes to Complex IV-dependent respiration and photobiomodulation-associated bioenergetic enhancement. Because mitochondrial content was not independently measured, the tissue findings cannot distinguish broader mitochondrial loss from protein-specific dysregulation.",
  "abstract_shown": true,
  "affiliations": [
    "Alzo Biosciences Inc., San Diego, CA 92121, USA",
    "Capillus LLC, Miami, FL 33131, USA"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 2,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Mohammad Golam Sabbir",
      "orcid": "0000-0002-0943-2542"
    },
    {
      "affs": [
        1
      ],
      "name": "Karin Hsiao"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/d8h00zb5xh6ze.bib",
  "cited_by": 0,
  "doi": "10.3390/cells15211941",
  "fulltext_url": null,
  "id": "d8h00zb5xh6ze",
  "issns": [
    "2073-4409"
  ],
  "landing_url": "https://www.mdpi.com/2073-4409/15/21/1941",
  "language": null,
  "licence": "CC-BY-4.0",
  "licence_label": "CC BY 4.0",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "1312|Mitochondrial Function and Pathology"
    ]
  ],
  "openalex": "W7223672181",
  "pdf_url": null,
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-25",
  "publisher": "MDPI AG",
  "ris": "https://research.draconitic.com/paper/d8h00zb5xh6ze.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:19:02Z",
      "native_id": "10.3390/cells15211941",
      "source": "crossref",
      "url": "https://www.mdpi.com/2073-4409/15/21/1941"
    }
  ],
  "subjects": [
    {
      "field": "biochemistry",
      "origin": "openalex:1312|Mitochondrial Function and Pathology",
      "subfield": "molecular-biology"
    }
  ],
  "title": "MT-CO2 Dysregulation in Alzheimer’s Disease and Its Modulation by Photobiomodulation: Implications for Mitochondrial Function",
  "title_text": "MT-CO2 Dysregulation in Alzheimer’s Disease and Its Modulation by Photobiomodulation: Implications for Mitochondrial Function",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:19:02Z",
  "url": "https://research.draconitic.com/paper/d8h00zb5xh6ze",
  "venue": "Cells",
  "versions": []
}