Protein oxidative modifications in the aging brain: consequence for the onset of neurodegenerative disease
Identifieur interne : 000149 ( Pmc/Checkpoint ); précédent : 000148; suivant : 000150Protein 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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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><p id="P2">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.</p></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">9423872</journal-id><journal-id journal-id-type="pubmed-jr-id">2548</journal-id><journal-id journal-id-type="nlm-ta">Free Radic Res</journal-id><journal-id journal-id-type="iso-abbrev">Free Radic. Res.</journal-id><journal-title-group><journal-title>Free radical research</journal-title></journal-title-group><issn pub-type="ppub">1071-5762</issn><issn pub-type="epub">1029-2470</issn></journal-meta><article-meta><article-id pub-id-type="pmid">20815785</article-id><article-id pub-id-type="pmc">3675897</article-id><article-id pub-id-type="doi">10.3109/10715762.2010.512040</article-id><article-id pub-id-type="manuscript">NIHMS478814</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Protein oxidative modifications in the aging brain: consequence for the onset of neurodegenerative disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Grimm</surname><given-names>Stefanie</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Hoehn</surname><given-names>Annika</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Davies</surname><given-names>Kelvin J.</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Grune</surname><given-names>Tilman</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Institute of Nutrition, Friedrich Schiller University Jena, Dornburger Straße 24, 07743 Jena, Germany</aff><aff id="A2"><label>2</label>Institute of Biological Chemistry and Nutrition, University Hohenheim, Garbenstrasse 28, 70593 Stuttgart, Germany</aff><aff id="A3"><label>3</label>Ethel Percy Andrus Gerontology Center of the Davis School of Gerontology; and Division of Molecular & Computational Biology, Department of Biological Sciences of the College of Letters, Arts & Sciences, the University of Southern California, Los Angeles, California 90089-0191, U.S.A.</aff><author-notes><corresp id="CR1">Address for correspondence: Tilman Grune Institute of Nutrition Friedrich Schiller University Jena Dornburger Straße 24, 07743 Jena, Germany Phone: +49 (0)3641 9496 70 Fax: +49 (0)3641 9496 72 <email>tilman.grune@uni-hohenheim.de</email> / <email>tilman.grune@uni-jena.de</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>30</day><month>5</month><year>2013</year></pub-date><pub-date pub-type="epub"><day>06</day><month>9</month><year>2010</year></pub-date><pub-date pub-type="ppub"><month>1</month><year>2011</year></pub-date><pub-date pub-type="pmc-release"><day>07</day><month>6</month><year>2013</year></pub-date><volume>45</volume><issue>1</issue><fpage>73</fpage><lpage>88</lpage><abstract><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><p id="P2">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.</p></abstract><kwd-group><kwd>oxidative stress</kwd><kwd>nitrative stress</kwd><kwd>neurodegenerative diseases</kwd><kwd>protein degradation</kwd><kwd>aging</kwd></kwd-group><funding-group><award-group><funding-source country="United States">National Institute of Environmental Health Sciences : NIEHS</funding-source><award-id>R56 ES003598 || ES</award-id></award-group><award-group><funding-source country="United States">National Institute of Environmental Health Sciences : NIEHS</funding-source><award-id>R01 ES003598 || ES</award-id></award-group><award-group><funding-source country="United States">National Institute on Aging : NIA</funding-source><award-id>R01 AG016256 || AG</award-id></award-group></funding-group></article-meta></front></pmc><affiliations><list><country><li>Allemagne</li><li>États-Unis</li></country><region><li>Bade-Wurtemberg</li><li>Californie</li><li>District de Stuttgart</li></region><settlement><li>Los Angeles</li><li>Stuttgart</li></settlement><orgName><li>Université de Californie du Sud</li></orgName></list><tree><country name="Allemagne"><noRegion><name sortKey="Grimm, Stefanie" sort="Grimm, Stefanie" uniqKey="Grimm S" first="Stefanie" last="Grimm">Stefanie Grimm</name></noRegion><name sortKey="Grimm, Stefanie" sort="Grimm, Stefanie" uniqKey="Grimm S" first="Stefanie" last="Grimm">Stefanie Grimm</name><name sortKey="Grune, Tilman" sort="Grune, Tilman" uniqKey="Grune T" first="Tilman" last="Grune">Tilman Grune</name><name sortKey="Hoehn, Annika" sort="Hoehn, Annika" uniqKey="Hoehn A" first="Annika" last="Hoehn">Annika Hoehn</name><name sortKey="Hoehn, Annika" sort="Hoehn, Annika" uniqKey="Hoehn A" first="Annika" last="Hoehn">Annika Hoehn</name></country><country name="États-Unis"><region name="Californie"><name sortKey="Davies, Kelvin J" sort="Davies, Kelvin J" uniqKey="Davies K" first="Kelvin J." last="Davies">Kelvin J. 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