The DOI matches its Crossref record; 149 of the 149 references it cites were found in a registry or an index.
Oxidative and nitrative stress in neurodegeneration
Open accessAbstract
Aerobes require oxygen for metabolism and normal free radical formation. As a result, maintaining the redox homeostasis is essential for brain cell survival due to their high metabolic energy requirement to sustain electrochemical gradients, neurotransmitter release, and membrane lipid stability. Further, brain antioxidant levels are limited compared to other organs and less able to compensate for reactive oxygen and nitrogen species (ROS/RNS) generation which contribute oxidative/nitrative stress (OS/NS). Antioxidant treatments such as vitamin E, minocycline, and resveratrol mediate neuroprotection by prolonging the incidence of or reversing OS and NS conditions. Redox imbalance occurs when the antioxidant capacity is overwhelmed, consequently leading to activation of alternate pathways that remain quiescent under normal conditions. If OS/NS fails to lead to adaptation, tissue damage and injury ensue, resulting in cell death and/or disease. The progression of OS/NS-mediated neurodegeneration along with contributions from microglial activation, dopamine metabolism, and diabetes comprise a detailed interconnected pathway. This review proposes a significant role for OS/NS and more specifically, lipid peroxidation (LPO) and other lipid modifications, by triggering microglial activation to elicit a neuroinflammatory state potentiated by diabetes or abnormal dopamine metabolism. Subsequently, sustained stress in the neuroinflammatory state overwhelms cellular defenses and prompts neurotoxicity resulting in the onset or amplification of brain damage.
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Cites
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Cited by
Dash, U. C., Bhol, N. K., Swain, S. K., Samal, R. R., Nayak, P. K., Raina, V., Panda, S. K., Kerry, R. G., Duttaroy, A. K., & Jena, A. B. (2025) · Acta Pharmaceutica Sinica B · doi:10.1016/j.apsb.2024.10.004 · Cited by 700
NADPH oxidase in brain injury and neurodegenerative disorders
Ma, M. W., Wang, J., Zhang, Q., Wang, R., Dhandapani, K. M., Vadlamudi, R. K., & Brann, D. W. (2017) · Molecular Neurodegeneration · doi:10.1186/s13024-017-0150-7 · Cited by 432
Tafani, M., Sansone, L., Limana, F., Arcangeli, T., De Santis, E., Polese, M., Fini, M., & Russo, M. A. (2016) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2016/3907147 · Cited by 373
Diabetes and Alzheimer’s disease crosstalk
Baglietto-Vargas, D., Shi, J., Yaeger, D. M., Ager, R., & LaFerla, F. M. (2016) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2016.03.005 · Cited by 256
Inflammasomes, hormesis, and antioxidants in neuroinflammation: Role of NRLP3 in Alzheimer disease
Pennisi, M., Crupi, R., Di Paola, R., Ontario, M. L., Bella, R., Calabrese, E. J., Crea, R., Cuzzocrea, S., & Calabrese, V. (2017) · Journal of Neuroscience Research · doi:10.1002/jnr.23986 · Cited by 157
Metadata
- Authors
- Cobb, C. A., & Cole, M. P.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2015-12
- Volume
- 84
- Pages
- 4-21
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W391900960
- Cited by
- 298
- References
- 149
- FWCI
- 17.62
- Type
- journal article
- Language
- en
- Open access
- green
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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