Protein oxidative modifications in the aging brain: consequence for the onset of neurodegenerative disease
Identifieur interne : 000242 ( Main/Exploration ); précédent : 000241; suivant : 000243Protein oxidative modifications in the aging brain: consequence for the onset of neurodegenerative disease
Auteurs : Stefanie Grimm [Allemagne] ; Annika Hoehn [Allemagne] ; Kelvin J. Davies [États-Unis] ; Tilman Grune [Allemagne]Source :
- Free radical research [ 1071-5762 ] ; 2010.
Abstract
The free radical theory of aging proposes the accumulation of altered, less active and toxic molecules of DNA, RNA, proteins and lipids caused by reactive oxygen species and reactive nitrogen species. Neurodegenerative disorders are characterized by an abnormal accumulation of oxidatively damaged macromolecules inside cells and in the extracellular space. Proteins involved in the formation of aggregates are β-amyloid, tau, α-synuclein, parkin, prion proteins and proteins containing polyglutamine. These abnormal aggregated proteins influence normal cellular metabolism. Additionally, deposition of abnormal proteins induces oxidative stress and proteasomal as well as mitochondrial dysfunction that ultimately lead to neuronal cell death.
In this review we focus on the impact of oxidative and nitrative stress in the aging brain and, consequently, on the generation of modified proteins, as these post-translational modifications are assumed to play an important role in the development of neurodegenerative diseases.
Url:
DOI: 10.3109/10715762.2010.512040
PubMed: 20815785
PubMed Central: 3675897
Affiliations:
- Allemagne, États-Unis
- Bade-Wurtemberg, Californie, District de Stuttgart
- Los Angeles, Stuttgart
- Université de Californie du Sud
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Le document en format XML
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<front><div type="abstract" xml:lang="en"><p id="P1">The free radical theory of aging proposes the accumulation of altered, less active and toxic molecules of DNA, RNA, proteins and lipids caused by reactive oxygen species and reactive nitrogen species. Neurodegenerative disorders are characterized by an abnormal accumulation of oxidatively damaged macromolecules inside cells and in the extracellular space. Proteins involved in the formation of aggregates are β-amyloid, tau, α-synuclein, parkin, prion proteins and proteins containing polyglutamine. These abnormal aggregated proteins influence normal cellular metabolism. Additionally, deposition of abnormal proteins induces oxidative stress and proteasomal as well as mitochondrial dysfunction that ultimately lead to neuronal cell death.</p>
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