Mitochondrial defects and oxidative stress in Alzheimer disease and Parkinson disease

Michael H. Yana, Xinglong Wang, Xiongwei Zhu

Research output: Contribution to journalReview articlepeer-review

349 Scopus citations

Abstract

Alzheimer disease (AD) and Parkinson disease (PD) are the two most common age-related neurode-generative 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 mitochon-drial homeostasis and function, in relationship with oxidative stress in the pathogenesis of AD and PD.

Original languageEnglish (US)
Pages (from-to)90-101
Number of pages12
JournalFree Radical Biology and Medicine
Volume62
DOIs
StatePublished - 2013
Externally publishedYes

Keywords

  • Alzheimer disease
  • DNA
  • Free radicals
  • Mitochondrial
  • Mitochondrial dynamics
  • Mitochondrial dysfunction
  • Oxidative stress
  • Parkinson disease

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

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