Cited by 720Mitochondrial Function and PathologyAlzheimer's disease research and treatmentsParkinson's Disease Mechanisms and Treatments

The DOI matches its Crossref record; 205 of the 209 references it cites were found in a registry or an index.

Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease

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Yan, Michael H., Wang, Xinglong, Zhu, Xiongwei·2013·Free Radical Biology and Medicine

Abstract

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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Crossref · 10.1016/j.freeradbiomed.2012.11.014

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  1. Bonifati, 2003, Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism, Science, 299, 256, 10.1126/science.1077209 · DOI

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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)
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
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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