Loss of mitochondrial function induces transcriptomic signatures of Alzheimer's Diseases in mice
Reduced mtCI activity was sufficient to induce the AD-like transcriptomic changes in brain. Residual mtCI function was sufficient to mediate neuroprotective effect of CP2, emphasizing a key role of mitochondria in AD development and treatment.
Authors
- Jarred J. Nesbitt
- Eugenia Trushina (ORCID: https://orcid.org/0000-0002-6291-2860)
- Mark Ostroot (ORCID: https://orcid.org/0009-0009-1253-2120)
- Priyanka Baloni (ORCID: https://orcid.org/0000-0002-3382-4941)
- Jesse C. Wiley (ORCID: https://orcid.org/0000-0002-1430-772X)
- Jens O. Watzlawik (ORCID: https://orcid.org/0000-0003-0610-0267)
- Huanyao Gao (ORCID: https://orcid.org/0000-0002-9441-9579)
- Wolfdieter Springer (ORCID: https://orcid.org/0000-0002-1178-3149)
- Cory C. Funk (ORCID: https://orcid.org/0000-0002-5229-9011)
- Kate N. Jensen (ORCID: https://orcid.org/0000-0003-4520-7956)
- Alexander Galkin
Institutions
- Sage Bionetworks (US)
- Mayo Clinic (US)
- Cornell University (US)
- Purdue University West Lafayette (US)
- WinnMed (US)
- Institute for Systems Biology (US)
- Yale University (US)
- Mayo Clinic in Arizona (US)
- Mayo Clinic in Florida (US)
- Weill Cornell Medicine (US)
Publication Details
- Journal
- Alzheimer s & Dementia
- Published
- 2025-12-01
- DOI
- https://doi.org/10.1002/alz70855_101111
- Primary Topic
- Alzheimer's disease research and treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00