The DOI matches its Crossref record; 138 of the 140 references it cites were found in a registry or an index.
Oxidative Stress and the Pathogenesis of Alzheimer's Disease
Open accessAbstract
Alzheimer's disease (AD) is the most common neurodegenerative disease that causes dementia in the elderly. Patients with AD suffer a gradual deterioration of memory and other cognitive functions, which eventually leads to a complete incapacity and death. A complicated array of molecular events has been implicated in the pathogenesis of AD. The major pathological characteristics of AD brains are the presence of senile plaques, neurofibrillary tangles, and neuronal loss. Growing evidence has demonstrated that oxidative stress is an important factor contributing to the initiation and progression of AD. However, the mechanisms that lead to the disruption of redox balance and the sources of free radicals remain elusive. The excessive reactive oxygen species may be generated from mechanisms such as mitochondria dysfunction and/or aberrant accumulation of transition metals, while the abnormal accumulation of Abeta and tau proteins appears to promote the redox imbalance. The resulted oxidative stress has been implicated in Abeta- or tau-induced neurotoxicity. In addition, evidence has suggested that oxidative stress may augment the production and aggregation of Abeta and facilitate the phosphorylation and polymerization of tau, thus forming a vicious cycle that promotes the initiation and progression of AD.
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“In the context of Aβ production, multiple investigations have revealed that oxidative stress leads to the formation of SPs by lowering α-secretase activity while increasing both βand γ-secretase activities [52].”
From Unlocking the Therapeutic Potential of Medicinal Plants for Alzheimer’s Disease: Preclinical to Clinical Trial Insights (2023) · cites this paper as [52]
In the citing paper
“However, when the hyperphosphorylated Tau protein is overexpressed (which is a pathophysiological indicator of AD) a depletion of these organelles has been evidenced, suggesting it is the cause of H2O2 and ROS increase [72,108,126].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [126]
In the citing paper
“Hydrogen peroxide seems to be the relevant actor in promoting excessive oxidation in neuronal cells.”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [126]
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Cites
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Oxidative Stress: A Key Modulator in Neurodegenerative Diseases
Singh, A., Kukreti, R., Saso, L., & Kukreti, S. (2019) · Molecules · doi:10.3390/molecules24081583 · Cited by 2,398
Oxidative stress and the amyloid beta peptide in Alzheimer’s disease
Cheignon, C., Tomas, M., Bonnefont-Rousselot, D., Faller, P., Hureau, C., & Collin, F. (2018) · Redox Biology · doi:10.1016/j.redox.2017.10.014 · Cited by 2,185
Bhatti, J. S., Bhatti, G. K., & Reddy, P. H. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.11.010 · Cited by 1,655
The role of oxidative stress in neurodegenerative diseases
Kim, G. H., Kim, J. E., Rhie, S. J., & Yoon, S. (2015) · Experimental Neurobiology · doi:10.5607/en.2015.24.4.325 · Cited by 1,355
Role of pro-inflammatory cytokines released from microglia in Alzheimer's disease.
(2015) · Europe PMC (PubMed Central) · doi:10.3978/j.issn.2305-5839.2015.03.49 · Cited by 1,288
Metadata
- Authors
- Zhao, Y., & Zhao, B.
- Affiliations
- Harbin Institute of Technology (CN)
- Chinese Academy of Sciences (CN)
- Corresponding author
- Zhao, Yan
- Zhao, Baolu
- ORCID
- Zhao, Yan
- Venue
- Oxidative Medicine and Cellular Longevity
- Publisher
- Wiley
- Published
- 2013
- Volume
- 2013
- Pages
- 1-10
- ISSN
- 1942-0994 (ISSN-L)
- 1942-0900
- PMC
- PMC3745981
- OpenAlex
- W2141262291
- Cited by
- 855
- References
- 140
- Citations by year
- 2026: 47 · 2025: 61 · 2024: 82 · 2023: 78 · 2022: 80 · 2021: 83 · 2020: 76 · 2019: 71 · 2018: 64 · 2017: 64 · 2016: 53 · 2015: 54 · 2014: 36 · 2013: 5
- FWCI
- 5.44
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- Oxidative Medicine and Cellular Longevity (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)
- Funders
- National Natural Science Foundation of China (30930036, 31201338, 30870587, 2009-3-93, 2011DXGJ14, Y200902, 2009147, 2006CB500706)
- Weihai Science and Technology Development Program (30930036, 31201338, 30870587, 2009-3-93, 2011DXGJ14, Y200902, 2009147, 2006CB500706)
- Harbin Institute of Technology (30930036, 31201338, 30870587, 2009-3-93, 2011DXGJ14, Y200902, 2009147, 2006CB500706)
- National Basic Research Program of China (30930036, 31201338, 30870587, 2009-3-93, 2011DXGJ14, Y200902, 2009147, 2006CB500706)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- Alzheimer's disease, oxidative stress, redox imbalance, reactive oxygen species, free radicals, mitochondrial dysfunction, amyloid-beta, tau protein, neurofibrillary tangles, amyloid plaques, neurotoxicity, neurodegeneration, dementia
- MeSH terms
- Alzheimer Disease, Humans, Reactive Oxygen Species, Oxidative Stress
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