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06:02
Detection of Neuritic Plaques in Alzheimer's Disease Mouse Model
Published on: July 26, 2011
Nucleic acid oxidation in Alzheimer disease
Paula I Moreira1, Akihiko Nunomura, Masao Nakamura
1Center for Neuroscience and Cell Biology, Institute of Physiology-Faculty of Medicine, University of Coimbra, Coimbra, Portugal.
Free Radical Biology & Medicine
|February 9, 2008
Summary
Oxidative stress damages nucleic acids in Alzheimer disease (AD). Mitochondrial and metal issues in AD increase this damage, overwhelming repair mechanisms.
Area of Science:
- Neuroscience
- Molecular Biology
- Biochemistry
Background:
- Oxidative stress is linked to Alzheimer disease (AD) pathophysiology.
- Neurons possess defense mechanisms against oxidative damage to ensure longevity.
- Accumulated nucleic acid oxidation in AD suggests increased oxidative stress or impaired repair.
Purpose of the Study:
- To review the role of oxidative stress in Alzheimer disease.
- To discuss the sources and mechanisms of nucleic acid oxidation and repair in AD.
- To present evidence of nucleic acid oxidation in AD.
Main Methods:
- Literature review of studies on oxidative stress and Alzheimer disease.
- Analysis of mechanisms of nucleic acid oxidation and repair.
- Examination of evidence for nucleic acid oxidation in AD.
Main Results:
- Mitochondrial and metal abnormalities are identified as key sources of oxidative stress in AD.
- Mechanisms of nucleic acid oxidation by reactive oxygen species are detailed.
- Evidence for nucleic acid oxidation in Alzheimer disease is presented.
Conclusions:
- Oxidative stress, particularly affecting nucleic acids, is a significant factor in Alzheimer disease.
- Mitochondrial dysfunction and metal dysregulation contribute to increased oxidative damage in AD.
- Impaired nucleic acid repair exacerbates oxidative damage in Alzheimer disease pathophysiology.
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