Impaired mitochondrial biogenesis, defective axonal transport of mitochondria, abnormal mitochondrial dynamics and synaptic degeneration in a mouse model of Alzheimer's disease
Open accessAbstract
Increasing evidence suggests that the accumulation of amyloid beta (Aβ) in synapses and synaptic mitochondria causes synaptic mitochondrial failure and synaptic degeneration in Alzheimer's disease (AD). The purpose of this study was to better understand the effects of Aβ in mitochondrial activity and synaptic alterations in neurons from a mouse model of AD. Using primary neurons from a well-characterized Aβ precursor protein transgenic (AβPP) mouse model (Tg2576 mouse line), for the first time, we studied mitochondrial activity, including axonal transport of mitochondria, mitochondrial dynamics, morphology and function. Further, we also studied the nature of Aβ-induced synaptic alterations, and cell death in primary neurons from Tg2576 mice, and we sought to determine whether the mitochondria-targeted antioxidant SS31 could mitigate the effects of oligomeric Aβ. We found significantly decreased anterograde mitochondrial movement, increased mitochondrial fission and decreased fusion, abnormal mitochondrial and synaptic proteins and defective mitochondrial function in primary neurons from AβPP mice compared with wild-type (WT) neurons. Transmission electron microscopy revealed a large number of small mitochondria and structurally damaged mitochondria, with broken cristae in AβPP primary neurons. We also found an increased accumulation of oligomeric Aβ and increased apoptotic neuronal death in the primary neurons from the AβPP mice relative to the WT neurons. Our results revealed an accumulation of intraneuronal oligomeric Aβ, leading to mitochondrial and synaptic deficiencies, and ultimately causing neurodegeneration in AβPP cultures. However, we found that the mitochondria-targeted antioxidant SS31 restored mitochondrial transport and synaptic viability, and decreased the percentage of defective mitochondria, indicating that SS31 protects mitochondria and synapses from Aβ toxicity.
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Synaptic mitochondria are particularly susceptible to dysfunction in AD, contributing to early impairments in plasticity and cognition.
“Evidence from experimental and clinical studies indicates that synaptic mitochondria are particularly susceptible to dysfunction in AD, contributing to early impairments in plasticity and cognition [55].”
From Toward a Unified Framework in Molecular Neurobiology of Alzheimer’s Disease: Revisiting the Pathophysiological Hypotheses (2026) · cites this paper as [55]
The Discussion (page unavailable) reports early preferential amyloid accumulation in synaptic mitochondria alongside impaired mitochondrial function, and describes evidence linking mitochondrial activity to a plasticity deficit. The Introduction links synaptic loss with cognitive decline. However, the paper does not establish that synaptic mitochondrial dysfunction causes early cognitive impairment in patients, and it says the mechanistic links remain unresolved. (LLM, conf=0.84)
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- Authors
- Calkins, M. J., Manczak, M., Mao, P., Shirendeb, U., & Reddy, P. H.
- Affiliations
- Oregon National Primate Research Center (US)
- Corresponding author
- Reddy, P. H.
- Venue
- Human Molecular Genetics
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-08-25
- Volume
- 20
- Issue
- 23
- Pages
- 4515-4529
- ISSN
- 0964-6906 (ISSN-L)
- 1460-2083
- PMC
- PMC3209824
- OpenAlex
- W2105442740
- Cited by
- 646
- References
- 16
- Citations by year
- 2026: 20 · 2025: 37 · 2024: 57 · 2023: 55 · 2022: 48 · 2021: 55 · 2020: 48 · 2019: 41 · 2018: 48 · 2017: 49 · 2016: 44 · 2015: 39 · 2014: 31 · 2013: 37 · 2012: 27
- FWCI
- 21.04
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Human Molecular Genetics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (RR 00163)
- National Institute on Aging (R01AG028072, AG028072)
- National Institute of Neurological Disorders and Stroke (P30NS061800)
- National Center for Research Resources (P51RR000163, K01RR000163, RR-00163.)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- Alzheimer's disease, amyloid-beta, mitochondrial biogenesis, mitochondrial dynamics, mitochondrial fission, mitochondrial fusion, synaptic degeneration, amyloid-beta oligomers, neuronal apoptosis, SS-31, mitochondria-targeted antioxidants, mitochondrial dysfunction, neurodegeneration
- MeSH terms
- Peptidyl-Prolyl Isomerase F, Adenosine Triphosphate, Alzheimer Disease, Animals, Axonal Transport, Cells, Cultured, Electron Transport Complex IV, Disease Models, Animal, Gene Expression Regulation, Hydrogen Peroxide, Mitochondria, Molecular Weight, Oligopeptides, RNA, Messenger, Synapses, Blotting, Western, Neurites, Amyloid beta-Protein Precursor, Apoptosis, Protein Structure, Quaternary, Cyclophilins, Mice, Peroxiredoxins
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