Oxidant Stress and Signal Transduction in the Nervous System with the PI 3-K, Akt, and mTOR Cascade
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Oxidative stress impacts multiple systems of the body and can lead to some of the most devastating consequences in the nervous system especially during aging. Both acute and chronic neurodegenerative disorders such as diabetes mellitus, cerebral ischemia, trauma, Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and tuberous sclerosis through programmed cell death pathways of apoptosis and autophagy can be the result of oxidant stress. Novel therapeutic avenues that focus upon the phosphoinositide 3-kinase (PI 3-K), Akt (protein kinase B), and the mammalian target of rapamycin (mTOR) cascade and related pathways offer exciting prospects to address the onset and potential reversal of neurodegenerative disorders. Effective clinical translation of these pathways into robust therapeutic strategies requires intimate knowledge of the complexity of these pathways and the ability of this cascade to influence biological outcome that can vary among disorders of the nervous system.
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Apoptosis in cells involves both an early phase consisting of exposure of membrane PS residues and a late phase involving destruction of genomic DNA.
“Apoptosis in cells involves both an early phase consisting of the exposure of membrane PS residues and a late phase that involves the destruction of genomic DNA [23, 45–47].”
From Tuberous Sclerosis Protein 2 (TSC2) Modulates CCN4 Cytoprotection During Apoptotic Amyloid Toxicity in Microglia (2013) · cites this paper as [23]
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Linking mitochondrial dysfunction, metabolic syndrome and stress signaling in Neurodegeneration
Jha, S. K., Jha, N. K., Kumar, D., Ambasta, R. K., & Kumar, P. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.06.015 · Cited by 122 · see citing works
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“mTOR is the catalytic component of two mTOR complexes termed mTOR Complex 1 (mTORC1) and mTOR Complex 2 (mTORC2) [22, 23].”
BackgroundSelf-citationWang, S., Zhong Chong, Z., Chen Shang, Y., & Maiese, K. (2013) · Current Neurovascular Research · doi:10.2174/156720213804805945 · Cited by 58 · see citing works
Self-citation
- Authors
- Maiese, K., Chong, Z. Z., Wang, S., & Shang, Y. C.
- Affiliations
- Rutgers Cancer Institute (US)
- Laboratory of Cellular and Molecular Signaling, Newark, NJ 07101, USA
- Corresponding author
- Maiese, Kenneth
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2012-10-26
- Volume
- 13
- Issue
- 11
- Pages
- 13830-13866
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC3509553
- OpenAlex
- W2002440118
- Cited by
- 109
- References
- 15
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 6 · 2023: 6 · 2022: 3 · 2021: 8 · 2020: 7 · 2019: 2 · 2018: 13 · 2017: 11 · 2016: 13 · 2015: 17 · 2014: 6 · 2013: 4 · 2012: 2
- FWCI
- 0.85
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- oxidative stress, neurodegenerative diseases, PI3K/AKT/mTOR pathway, signal transduction, nervous system aging, apoptosis, autophagy, Alzheimer's disease, Parkinson's disease, Huntington's disease, tuberous sclerosis complex, cerebral ischemia, diabetes mellitus, therapeutic target
- MeSH terms
- Animals, Cell Survival, Humans, Nervous System, Signal Transduction, Cell Death, Oxidative Stress, Neurodegenerative Diseases, Phosphatidylinositol 3-Kinases, Diabetes Complications, Proto-Oncogene Proteins c-akt, TOR Serine-Threonine Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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