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Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease
Open accessAbstract
Alzheimer disease (AD) and Parkinson disease (PD) are the two most common age-related neurodegenerative diseases characterized by prominent neurodegeneration in selective neural systems. Although a small fraction of AD and PD cases exhibit evidence of heritability, among which many genes have been identified, the majority are sporadic without known causes. Molecular mechanisms underlying neurodegeneration and pathogenesis of these diseases remain elusive. Convincing evidence demonstrates oxidative stress as a prominent feature in AD and PD and links oxidative stress to the development of neuronal death and neural dysfunction, which suggests a key pathogenic role for oxidative stress in both AD and PD. Notably, mitochondrial dysfunction is also a prominent feature in these diseases, which is likely to be of critical importance in the genesis and amplification of reactive oxygen species and the pathophysiology of these diseases. In this review, we focus on changes in mitochondrial DNA and mitochondrial dynamics, two aspects critical to the maintenance of mitochondrial homeostasis and function, in relationship with oxidative stress in the pathogenesis of AD and PD.
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“It has been proposed that ROS, which are considered markers of oxidative stress, are generated in the cytoplasm of neurons and can cause damage to key cellular components, including DNA, proteins, and lipids, leading to neuronal dysfunction and death (56, 59, 60).”
From Molecular Basis for Increased Risk for Late-onset Alzheimer Disease Due to the Naturally Occurring L28P Mutation in Apolipoprotein E4 (2014) · cites this paper as [60]
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“An increasing body of research indicates that ROS generation exacerbates α-synuclein misfolding in the brain, resulting in PD and other synaptic proteinopathies [37,38].”
From Neuroprotective Effects of Bifidobacterium breve CCFM1067 in MPTP-Induced Mouse Models of Parkinson’s Disease (2022) · cites this paper as [37]
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“In clinical studies, probiotics have been shown to lower the development of α-synuclein aggregates by lowering ROS levels, thereby improving the condition of patients with PD [37,39].”
From Neuroprotective Effects of Bifidobacterium breve CCFM1067 in MPTP-Induced Mouse Models of Parkinson’s Disease (2022) · cites this paper as [37]
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Self-citationSaurons-nous jamais ce qui provoque le vieillissement ?
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Metadata
- Authors
- Yan, M. H., Wang, X., & Zhu, X.
- Affiliations
- Case Western Reserve University (US)
- Corresponding author
- Wang, Xinglong
- Zhu, Xiongwei
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2013-09
- Volume
- 62
- Pages
- 90-101
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3744189
- OpenAlex
- W2027783468
- Cited by
- 718
- References
- 209
- Citations by year
- 2026: 14 · 2025: 34 · 2024: 73 · 2023: 56 · 2022: 69 · 2021: 67 · 2020: 53 · 2019: 47 · 2018: 53 · 2017: 71 · 2016: 54 · 2015: 49 · 2014: 48 · 2013: 30
- FWCI
- 16.31
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- the National Institutes of Health (AG031852, NS071184)
- Alzheimer's Association (IIRG-10–173358)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- Alzheimer's disease, Parkinson's disease, mitochondrial dysfunction, oxidative stress, mitochondrial DNA, mitochondrial dynamics, reactive oxygen species, neurodegeneration, mitochondrial homeostasis
- MeSH terms
- Alzheimer Disease, Humans, Mitochondria, Nerve Degeneration, Neurons, Parkinson Disease, Amyloid beta-Peptides, Cell Death, Reactive Oxygen Species, Oxidative Stress
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