Mitochondrial dysfunction and oxidative stress: A contributing link to acquired epilepsy?
Open accessAbstract
Mitochondrial dysfunction and oxidative stress contribute to several neurologic disorders and have recently been implicated in acquired epilepsies such as temporal lobe epilepsy (TLE). Acquired epilepsy is typically initiated by a brain injury followed by a "latent period" whereby molecular, biochemical and other cellular alterations occur in the brain leading to chronic epilepsy. Mitochondrial dysfunction and oxidative stress are emerging as factors that not only occur acutely as a result of precipitating injuries such as status epilepticus (SE), but may also contribute to epileptogenesis and chronic epilepsy. Mitochondria are the primary site of reactive oxygen species (ROS) making them uniquely vulnerable to oxidative damage that may affect neuronal excitability and seizure susceptibility. This mini-review provides an overview of evidence suggesting the role of mitochondrial dysfunction and oxidative stress as acute consequences of injuries that are known to incite chronic epilepsy and their involvement in the chronic stages of acquired epilepsy.
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Oxidative DNA damage and mitochondrial dysfunction are thought to contribute to neurodegeneration of AD, vascular dementia, HD, PD and epilepsy.
“Oxidative DNA damage and mitochondrial dysfunction are thought to contribute to the neurodegeneration of AD [75,76], vascular dementia [77], HD [78], PD [79] and epilepsy [80].”
From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [80]
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- Authors
- Waldbaum, S., & Patel, M.
- Affiliations
- University of Colorado Anschutz (US)
- Corresponding author
- Patel, Manisha
- ORCID
- Patel, Manisha
- Venue
- Journal of Bioenergetics and Biomembranes
- Published
- 2010-12
- Volume
- 42
- Issue
- 6
- Pages
- 449-455
- ISSN
- 0145-479X (ISSN-L)
- 1573-6881
- PMC
- PMC3102435
- OpenAlex
- W1969430202
- Cited by
- 264
- References
- 0
- Citations by year
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- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Bioenergetics and Biomembranes (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS039587)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology › Diet and metabolism studies
- Keywords
- mitochondrial dysfunction, oxidative stress, acquired epilepsy, temporal lobe epilepsy, epileptogenesis, status epilepticus, reactive oxygen species, chronic epilepsy, brain injury, neuronal excitability, seizure susceptibility
- MeSH terms
- Energy Metabolism, Epilepsy, Temporal Lobe, Humans, Mitochondria, Neurons, Oxidation-Reduction, Reactive Oxygen Species, Oxidative Stress
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