Identification and Characterization of Amyloid-β Accumulation in Synaptic Mitochondria
Abstract
Mitochondrial and synaptic dysfunction is an early pathological feature of Alzheimer's disease (AD). Accumulation of amyloid beta-peptide (Aβ) in mitochondria, particularly in synaptic mitochondria, potentiates and amplifies synaptic injury and disruption of synaptic transmission, leading to synaptic dysfunction and ultimately to synaptic failure. Thus, determination of the presence and levels of Aβ in synaptic mitochondria associated with amyloid pathology is important for studying mitochondrial amyloid pathology. Here, we present a detailed methodology for the isolation of synaptic mitochondria from brain tissues and the determination of Aβ levels in the isolated mitochondria as well as ultrastructural localization of synaptic mitochondrial Aβ. These methods have been used successfully for the identification and characterization of Aβ accumulation in synaptic mitochondria from mouse brains derived from transgenic AD mouse model. Additionally, we comprehensively discuss the sample preparation, experimental details, our unique procedures, optimization of parameters, and troubleshooting.
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Mitochondria are the primary producers of intracellular reactive oxygen species and are susceptible to oxidative stress caused by toxic metabolites such as β-amyloid.
“Mitochondria not only generate ATP but also act as the primary producers of intracellular reactive oxygen species (ROS) and are susceptible to oxidative stress caused by various toxic metabolites, such as β‐amyloid (Aβ) [3, 4].”
From Aerobic exercise improves astrocyte mitochondrial quality and transfer to neurons in a mouse model of Alzheimer's disease (2025) · cites this paper as [4]
Cites
RAGE-mediated signaling contributes to intraneuronal transport of amyloid-β and neuronal dysfunction
Takuma, K., Fang, F., Zhang, W., Yan, S., Fukuzaki, E., Du, H., Sosunov, A., McKhann, G., Funatsu, Y., Nakamichi, N., et al. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0905686106 · Cited by 290 · see citing works
Self-citationAlzheimer's APP mangles mitochondria
Lin, M. T., & Beal, M. F. (2006) · Nature Medicine · doi:10.1038/nm1106-1241 · Cited by 143 · see citing works
Mitochondrial Aβ A potential cause of metabolic dysfunction in Alzheimer's disease
Chen, X., & Yan, S. D. (2006) · IUBMB Life · doi:10.1080/15216540601047767 · Cited by 96 · see citing works
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Cai, J., Chen, Y., She, Y., He, X., Feng, H., Sun, H., Yin, M., Gao, J., Sheng, C., Li, Q., et al. (2025) · Brain Pathology · doi:10.1111/bpa.13316 · Cited by 30 · see citing works
- Authors
- Yan, S. F., Akhter, F., Sosunov, A. A., & Yan, S. S.
- Affiliations
- University of Kansas (US)
- Columbia University (US)
- Corresponding author
- Yan, Shi Fang
- Yan, Shirley ShiDu
- Venue
- Methods in Molecular Biology
- Publisher
- Springer New York
- Published
- 2018
- Volume
- 1779
- Pages
- 415-433
- ISSN
- 1064-3745 (ISSN-L)
- 1940-6029
- OpenAlex
- W2805392360
- Cited by
- 15
- References
- 3
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 2 · 2023: 2 · 2021: 1 · 2020: 5 · 2019: 1 · 2018: 1
- FWCI
- 6.65
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Methods in molecular biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (R37AG037319, R01AG053041, R01AG044793)
- National Institute of Neurological Disorders and Stroke (R01NS089116)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- amyloid-beta, synaptic mitochondria, Alzheimer's disease, synaptic dysfunction, mitochondrial isolation, ultrastructural localization, transgenic mouse model, synaptic injury
- MeSH terms
- Alzheimer Disease, Animals, Brain, Centrifugation, Density Gradient, Disease Models, Animal, Humans, Mice, Transgenic, Microscopy, Electron, Mitochondria, Synapses, Amyloid beta-Peptides, Mice
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