The role of oxidative stress in neurodegenerative diseases
Open accessAbstract
Oxidative stress is induced by an imbalanced redox states, involving either excessive generation of reactive oxygen species (ROS) or dysfunction of the antioxidant system. The brain is one of organs especially vulnerable to the effects of ROS because of its high oxygen demand and its abundance of peroxidation-susceptible lipid cells. Previous studies have demonstrated that oxidative stress plays a central role in a common pathophysiology of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. Antioxidant therapy has been suggested for the prevention and treatment of neurodegenerative diseases, although the results with regard to their efficacy of treating neurodegenerative disease have been inconsistent. In this review, we will discuss the role of oxidative stress in the pathophysiology of neurodegenerative diseases and in vivo measurement of an index of damage by oxidative stress. Moreover, the present knowledge on antioxidant in the treatment of neurodegenerative diseases and future directions will be outlined.
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Oxidative stress is part of AD pathology as Aβ42 neurotoxicity leads to induction of reactive oxygen species and other free radicals, which may escalate production and deposition of Aβ and phosphorylation and polymerization of tau.
“Oxidative stress is part of AD pathology as Aβ42 neurotoxicity leads to induction of reactive oxygen species and other free radicals, which in turn may escalate production and deposition of Aβ and phosphorylation and polymerization of tau (Kim et al., 2015).”
From Alzheimer's-associated PU.1 expression levels regulate microglial inflammatory response (2021) · cites this paper as Kim et al., 2015
The Alzheimer’s disease section says Aβ accumulation may increase oxidative stress and ROS, while oxidative stress can increase Aβ production and deposition and promote tau phosphorylation. It does not specifically identify Aβ42 as the cause or say that oxidative stress promotes tau polymerization. Page numbers were not provided in our copy. (LLM, conf=0.87)
Experimental — accuracy not yet measuredOxidative stress acts as a vehicle for deposition and accumulation of amyloid β in AD through production of reactive oxygen species.
“Evidence indicates that, through production of reactive oxygen species, oxidative stress acts as vehicle for deposition and accumulation of amyloid β (Aβ) in AD (Kim et al., 2015).”
From Effect of Probiotic Supplementation on Cognitive Function and Metabolic Status in Alzheimer's Disease: A Randomized, Double-Blind and Controlled Trial (2016) · cites this paper as Kim et al., 2015
Various investigations have shown that nutraceuticals are capable of fulfilling neuroprotective functions on molecular mechanisms that trigger Alzheimer's disease, acting as antioxidants or anti-neuroinflammatory drugs, affecting aggregation of β amyloid peptides, hyperphosphorylation of Tau protein, and decrease of acetylcholine in cholinergic neurons.
“Various investigations have shown that nutraceuticals are capable of fulfilling neuroprotective functions on molecular mechanisms that trigger AD, acting as antioxidants or anti-neuroinflammatory drugs, taking effect on the aggregation of β amyloid peptides, the hyperphosphorylation of the Tau protein and the decrease of the neurotransmitter ACh in cholinergic neurons [70,71,72]”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [72]
In Alzheimer's disease, excessive oxidative stress manifests from the early stages of the disease.
“Particularly for AD, excessive OS manifests itself from the early stages of the disease [72,125].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [72]
ROS are postulated to be the main cause of neurological deterioration, triggering pathologies such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.
“ROS have been postulated to be the main cause of neurological deterioration, triggering pathologies such as AD, Parkinson’s disease (PD), and Huntington’s disease (HD) [72,116,124].”
From Multi-Target Mechanisms of Phytochemicals in Alzheimer’s Disease: Effects on Oxidative Stress, Neuroinflammation and Protein Aggregation (2022) · cites this paper as [72]
Hydrogen peroxide is the relevant actor in promoting excessive oxidation in neuronal cells.
“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 [72]
When hyperphosphorylated Tau protein is overexpressed, peroxisome depletion occurs, suggesting that this depletion causes H2O2 and ROS increase.
“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 [72]
A possible linkage between oxidative stress and neurodegenerative disorders such as Huntington disease has been shown in literature.
“A possible linkage between oxidative stress and neurodegenerative disorders such as HD has been shown in literature”
From Nanotechnology: A Promising Approach for Delivery of Neuroprotective Drugs (2020) · cites this paper as Kim et al., 2015
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- Authors
- Kim, G. H., Kim, J. E., Rhie, S. J., & Yoon, S.
- Affiliations
- Ewha Womans University (KR)
- Corresponding author
- Yoon, Sujung
- Venue
- Experimental Neurobiology
- Published
- 2015-12-30
- Volume
- 24
- Issue
- 4
- Pages
- 325-340
- ISSN
- 1226-2560 (ISSN-L)
- 2093-8144
- PMC
- PMC4688332
- OpenAlex
- W2185348657
- Cited by
- 1,355
- References
- 143
- Citations by year
- 2026: 53 · 2025: 108 · 2024: 142 · 2023: 124 · 2022: 135 · 2021: 167 · 2020: 187 · 2019: 171 · 2018: 103 · 2017: 114 · 2016: 49 · 2013: 1
- FWCI
- 9.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Experimental Neurobiology (publishedVersion)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- Funders
- MSIP (B0132-15-1001)
- Topics
- Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- oxidative stress, neurodegenerative diseases, reactive oxygen species, antioxidant defense, antioxidant therapy, Alzheimer's disease, Parkinson's disease, lipid peroxidation, oxidative damage biomarkers, redox imbalance
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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