Cited by 863Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchRedox biology and oxidative stress

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Oxidative Stress and the Pathogenesis of Alzheimer's Disease

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Zhao, Yan, Zhao, Baolu·2013·Oxidative Medicine and Cellular Longevity

DOI 10.1155/2013/316523PMC PMC3745981

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Abstract

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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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
DOI: 10.1155/2013/316523
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
Licence: cc-by
creativecommons.org/licenses/by/3.0/ (unspecified)
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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