The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Rapid cell death is preceded by amyloid plaque-mediated oxidative stress
Open accessAbstract
Neuronal loss is the ultimate outcome in a variety of neurodegenerative diseases and central nerve system disorders. Understanding the sequelae of events that leads to cell death would provide insight into neuroprotective approaches. We imaged neurons in the living brain of a mouse model of Alzheimer's disease that overexpresses mutant human amyloid precursor protein and presenilin 1 and followed the death of individual neurons in real time. This mouse model exhibited limited neurodegeneration and atrophy, but we were able to identify a small fraction of vulnerable cells that would not have been detectable by using standard approaches. By exploiting a genetically encoded reporter of oxidative stress, we identified susceptible neurons by their increased redox potential. The oxidative stress was most dramatic in neurites near plaques, propagated to cell bodies, and preceded activation of caspases that led to cell death within 24 h. Thus, local oxidative stress surrounding plaques contributes to long-range toxicity and selective neuronal death in Alzheimer's disease.
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“and local oxidative stress surrounding plaques has been proposed as a potential mechanism contributing to selective neuronal death [37].”
From Neuron Loss in Alzheimer’s Disease: Translation in Transgenic Mouse Models (2020) · cites this paper as [37]
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Cites
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Research works printed but not linked: 1
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Oxidative stress and mitochondrial dysfunction in Alzheimer’s disease
Wang, X., Wang, W., Li, L., Perry, G., Lee, H.-G., & Zhu, X. (2014) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2013.10.015 · Cited by 1,357
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Glial Lipid Droplets and ROS Induced by Mitochondrial Defects Promote Neurodegeneration
Liu, L., Zhang, K., Sandoval, H., Yamamoto, S., Jaiswal, M., Sanz, E., Li, Z., Hui, J., Graham, B. H., Quintana, A., et al. (2015) · Cell · doi:10.1016/j.cell.2014.12.019 · Cited by 876
Understanding mechanisms of antioxidant action in health and disease
Halliwell, B. B. (2023) · Nature Reviews Molecular Cell Biology · doi:10.1038/s41580-023-00645-4 · Cited by 709
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Metadata
- Authors
- Xie, H., Hou, S., Jiang, J., Sekutowicz, M., Kelly, J., & Bacskai, B. J.
- Affiliations
- Massachusetts General Hospital (US)
- Tsinghua University (CN)
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2013-04-22
- Volume
- 110
- Issue
- 19
- Pages
- 7904-7909
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC3651444
- OpenAlex
- W2086831255
- Cited by
- 172
- References
- 29
- Citations by year
- 2026: 8 · 2025: 13 · 2024: 15 · 2023: 11 · 2022: 12 · 2021: 14 · 2020: 16 · 2019: 17 · 2018: 11 · 2017: 8 · 2016: 11 · 2015: 13 · 2014: 14 · 2013: 8
- FWCI
- 10.65
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG024688, R01AG024688)
- National Institute of Biomedical Imaging and Bioengineering (EB 000768, R01EB000768)
- National Center for Research Resources (S10RR025645)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid plaques, oxidative stress, neuronal cell death, presenilin 1, amyloid precursor protein, caspase activation, neurodegeneration, neuroprotection
- MeSH terms
- Alzheimer Disease, Animals, Atrophy, Gene Expression Regulation, Image Processing, Computer-Assisted, Mice, Transgenic, Neurons, Oxidation-Reduction, Time Factors, Cell Death, Oxidative Stress, Caspases, Green Fluorescent Proteins, Mice, Plaque, Amyloid
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