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Cited by 106Mitochondrial Function and PathologyAlzheimer's disease research and treatmentsAutophagy in Disease and Therapy

Mitochondria, Cybrids, Aging, and Alzheimer's Disease

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Swerdlow, R.H., Koppel, S., Weidling, I., Hayley, C., Ji, Y., Wilkins, H.M.·2017·Progress in Molecular Biology and Translational Science
DOI 10.1016/bs.pmbts.2016.12.017PMC PMC5864124
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Abstract

Mitochondrial and bioenergetic function change with advancing age and may drive aging phenotypes. Mitochondrial and bioenergetic changes are also documented in various age-related neurodegenerative diseases, including Alzheimer's disease (AD). In some instances AD mitochondrial and bioenergetic changes are reminiscent of those observed with advancing age but are greater in magnitude. Mitochondrial and bioenergetic dysfunction could, therefore, link neurodegeneration to brain aging. Interestingly, mitochondrial defects in AD patients are not brain-limited, and mitochondrial function can be linked to classic AD histologic changes including amyloid precursor protein processing to beta amyloid. Also, transferring mitochondria from AD subjects to cell lines depleted of endogenous mitochondrial DNA (mtDNA) creates cytoplasmic hybrid (cybrid) cell lines that recapitulate specific biochemical, molecular, and histologic AD features. Such findings have led to the formulation of a "mitochondrial cascade hypothesis" that places mitochondrial dysfunction at the apex of the AD pathology pyramid. Data pertinent to this premise are reviewed.

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  • Cybrid models demonstrate that mitochondrial defects alone can recapitulate key AD phenotypes, including decreased complex IV activity, increased ROS generation, synaptic dysfunction, and enhanced Aβ and phosphorylated tau accumulation.

    “Evidence from cytoplasmic hybrid (cybrid) models, where mitochondria from AD patients are transferred into mtDNA-depleted cells, demonstrates that mitochondrial defects alone can recapitulate key AD phenotypes, including decreased complex IV activity, increased ROS generation, synaptic dysfunction, and enhanced Aβ and phosphorylated tau accumulation [59, 60].”

    From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [59]

    The AD Cybrid Experiments section reports reduced complex IV (COX) activity, increased oxidative-stress markers, and increased Aβ levels in AD cybrids. It does not report synaptic dysfunction or phosphorylated tau accumulation in those cybrids, and oxidative-stress markers do not directly establish increased ROS generation. The Implications and Limitations section says mitochondrial function can contribute to these changes, rather than demonstrating that mitochondrial defects alone cause them. (LLM, conf=0.88)

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Authors
Swerdlow, R. H., Koppel, S., Weidling, I., Hayley, C., Ji, Y., & Wilkins, H. M.
Affiliations
University of Kansas (US)
Corresponding author
Swerdlow, R.H.
ORCID
Venue
Progress in Molecular Biology and Translational Science
Publisher
Elsevier
Published
2017
Volume
146
Pages
259-302
ISSN
1877-1173 (ISSN-L)
DOI
10.1016/bs.pmbts.2016.12.017
PMC
PMC5864124
OpenAlex
W2584978674
Cited by
106
References
41
Citations by year
2026: 9 · 2025: 5 · 2024: 7 · 2023: 16 · 2022: 12 · 2021: 19 · 2020: 17 · 2019: 11 · 2018: 6 · 2017: 3 · 2016: 1
FWCI
12.53
Type
book chapter
Language
en
Open access
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Progress in molecular biology and translational science (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (P30AG035982)
  • Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32HD057850)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
Keywords
mitochondria, cybrids, Alzheimer's disease, brain aging, mitochondrial dysfunction, bioenergetics, mitochondrial DNA, amyloid precursor protein, amyloid-beta, age-related neurodegeneration
MeSH terms
Aging, Alzheimer Disease, Animals, Cytoplasm, DNA, Mitochondrial, Humans, Mitochondria, Inheritance Patterns

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