Cited by 1,355Antioxidant Activity and Oxidative StressRedox biology and oxidative stressParkinson's Disease Mechanisms and Treatments

The role of oxidative stress in neurodegenerative diseases

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Kim, Geon Ha, Kim, Jieun E., Rhie, Sandy Jeong, Yoon, Sujung·2015·Experimental Neurobiology

Abstract

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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Crossref · 10.5607/en.2015.24.4.325

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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 measured
  • Oxidative 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).”
  • 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]”
  • 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].”
  • 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].”

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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
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
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

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