Reactive oxygen species and the neuronal fate
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Aberrant or elevated levels of reactive oxygen species (ROS) can mediate deleterious cellular effects, including neuronal toxicity and degeneration observed in the etiology of a number of pathological conditions, including Alzheimer's and Parkinson's diseases. Nevertheless, ROS can be generated in a controlled manner and can regulate redox sensitive transcription factors such as NFκB, AP-1 and NFAT. Moreover, ROS can modulate the redox state of tyrosine phosphorylated proteins, thereby having an impact on many transcriptional networks and signaling cascades important for neurogenesis. A large body of literature links the controlled generation of ROS at low-to-moderate levels with the stimulation of differentiation in certain developmental programs such as neurogenesis. In this regard, ROS are involved in governing the acquisition of the neural fate-from neural induction to the elaboration of axons. Here, we summarize and discuss the growing body of literature that describe a role for ROS signaling in neuronal development.
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Evidence for oxidative stress has been found in patients with schizophrenia, including increased lipid and protein oxidation in blood, CSF and post-mortem tissue, altered plasma antioxidants, and altered CSF superoxide dismutase-1 levels.
“Evidence for oxidative stress has been found in patients with schizophrenia, including increased lipid and protein oxidation in blood, cerebrospinal fluid (CSF) and post-mortem tissue 36,37 , as well as altered levels of plasma antioxidants (such as vitamins C and E, catalase, GSH and GSH-peroxidase) 36,38 and CSF superoxide dismutase-1 levels 39 .”
From Linking early-life NMDAR hypofunction and oxidative stress in schizophrenia pathogenesis (2016) · cites this paper as [37]
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- Authors
- Kennedy, K. A. M., Sandiford, S. D. E., Skerjanc, I. S., & Li, S. S.-C.
- Affiliations
- Western University (CA)
- University of Ottawa (CA)
- Corresponding author
- Li, Shawn S.-C.
- ORCID
- Li, Shawn S.-C.
- Venue
- Cellular and Molecular Life Sciences
- Published
- 2011-09-23
- Volume
- 69
- Issue
- 2
- Pages
- 215-221
- ISSN
- 1420-682X (ISSN-L)
- 1420-9071
- PMC
- PMC11114775
- OpenAlex
- W2021375247
- Cited by
- 89
- References
- 84
- Citations by year
- 2026: 3 · 2025: 5 · 2024: 4 · 2023: 8 · 2022: 4 · 2021: 6 · 2020: 3 · 2019: 5 · 2018: 3 · 2017: 5 · 2016: 9 · 2015: 7 · 2014: 13 · 2013: 8 · 2012: 6
- FWCI
- 0.78
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cellular and Molecular Life Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Canada Research Chairs
- Canadian Institutes of Health Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Keywords
- reactive oxygen species, neuronal fate, neurogenesis, neuronal differentiation, redox signaling, redox-sensitive transcription factors, NF-κB, AP-1, NFAT, tyrosine phosphorylation, oxidative stress, neurotoxicity, neural induction, axon development, Alzheimer's disease, Parkinson's disease
- MeSH terms
- Animals, Female, Humans, Male, Nervous System, Neurons, Signal Transduction, Reactive Oxygen Species, NADPH Oxidases, Mice, Neurogenesis
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