Crosslinking of α-synuclein by advanced glycation endproducts — an early pathophysiological step in Lewy body formation?
Identifieur interne : 000217 ( France/Analysis ); précédent : 000216; suivant : 000218Crosslinking of α-synuclein by advanced glycation endproducts — an early pathophysiological step in Lewy body formation?
Auteurs : G. Münch [Allemagne] ; H. J. Lüth [Allemagne] ; A. Wong [Allemagne] ; Th. Arendt [Allemagne] ; E. Hirsch [France] ; R. Ravid [Pays-Bas] ; P. Riederer [Allemagne]Source :
- Journal of Chemical Neuroanatomy [ 0891-0618 ] ; 2000.
English descriptors
- KwdEn :
Abstract
An excess of reactive carbonyl compounds (carbonyl stress) and their reaction products, advanced glycation endproducts (AGEs), are thought to play a decisive role in the pathogenesis of neurodegenerative disorders and Parkinson's disease (PD) in particular. Accumulation of AGEs in various intracellular pathological hallmarks of PD, such as Lewy bodies, densely crosslinked intracellular protein deposits formed from neurofilament components and α-synuclein, have already been described in patients in advanced stages of the disease. There is, however, no indication of the involvement of AGE-induced crosslinking of α-synuclein in very early stages of the disease. In this study, we observed that AGEs and α-synuclein are similarly distributed in very early Lewy bodies in the human brain in cases with incidental Lewy body disease. These cases might be viewed as pre-Parkinson patients, i.e. patients who came for autopsy before the possible development of clinical signs of PD. AGEs are both markers of transition metal induced oxidative stress as well as, inducers of protein crosslinking and free radical formation by chemical and cellular processes. Thus, it is likely that AGE promoted formation of Lewy bodies reflects very early causative changes rather than late epiphenomenons of PD.
Url:
DOI: 10.1016/S0891-0618(00)00096-X
Affiliations:
- Allemagne, France, Pays-Bas
- Bavière, District de Basse-Franconie, District de Leipzig, Hollande-Septentrionale, Saxe (Land)
- Amsterdam, Leipzig, Paris, Wurtzbourg
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ISTEX:28033EAD641FEBD0F290CEEF1C2713A85289BE31Le document en format XML
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Münch</name><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Neuroimmunological Cell Biology Group, Interdisciplinary Center for Clinical Research (IZKF), University of Leipzig, Leipzig</wicri:regionArea><placeName><region type="land" nuts="1">Saxe (Land)</region><region type="district" nuts="2">District de Leipzig</region><settlement type="city">Leipzig</settlement></placeName></affiliation></author><author><name sortKey="Luth, H J" sort="Luth, H J" uniqKey="Luth H" first="H. J." last="Lüth">H. J. 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Arendt</name><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Paul-Flechsig-Institut für Hirnforschung, University of Leipzig, Leipzig</wicri:regionArea><placeName><region type="land" nuts="1">Saxe (Land)</region><region type="district" nuts="2">District de Leipzig</region><settlement type="city">Leipzig</settlement></placeName></affiliation></author><author><name sortKey="Hirsch, E" sort="Hirsch, E" uniqKey="Hirsch E" first="E." last="Hirsch">E. Hirsch</name><affiliation wicri:level="1"><country xml:lang="fr">France</country><wicri:regionArea>Inserm U 289, Mécanismes et Conséquences de la Mort Neuronale, Hôpital de la Salpêtrière, Paris</wicri:regionArea><placeName><settlement type="city">Paris</settlement></placeName></affiliation></author><author><name sortKey="Ravid, R" sort="Ravid, R" uniqKey="Ravid R" first="R." last="Ravid">R. Ravid</name><affiliation wicri:level="3"><country xml:lang="fr">Pays-Bas</country><wicri:regionArea>Netherlands Brain Bank, Amsterdam</wicri:regionArea><placeName><settlement type="city">Amsterdam</settlement><region nuts="2" type="province">Hollande-Septentrionale</region></placeName></affiliation></author><author><name sortKey="Riederer, P" sort="Riederer, P" uniqKey="Riederer P" first="P." last="Riederer">P. Riederer</name><affiliation wicri:level="3"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Clinical Neurochemistry, Department of Psychiatry, University School of Medicine, University of Würzburg, Würzburg</wicri:regionArea><placeName><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Basse-Franconie</region><settlement type="city">Wurtzbourg</settlement></placeName></affiliation><affiliation><wicri:noCountry code="no comma">Corresponding author. Tel.: +49-931-2017720; fax: +49-931-2017722</wicri:noCountry></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Allemagne</country></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Chemical Neuroanatomy</title><title level="j" type="abbrev">CHENEU</title><idno type="ISSN">0891-0618</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000">2000</date><biblScope unit="volume">20</biblScope><biblScope unit="issue">3–4</biblScope><biblScope unit="page" from="253">253</biblScope><biblScope unit="page" to="257">257</biblScope></imprint><idno type="ISSN">0891-0618</idno></series><idno type="istex">28033EAD641FEBD0F290CEEF1C2713A85289BE31</idno><idno type="DOI">10.1016/S0891-0618(00)00096-X</idno><idno type="PII">S0891-0618(00)00096-X</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0891-0618</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Advanced glycation endproducts</term><term>Lewy bodies</term><term>Neurodegeneration</term><term>Oxidative stress</term><term>Parkinson's disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">An excess of reactive carbonyl compounds (carbonyl stress) and their reaction products, advanced glycation endproducts (AGEs), are thought to play a decisive role in the pathogenesis of neurodegenerative disorders and Parkinson's disease (PD) in particular. Accumulation of AGEs in various intracellular pathological hallmarks of PD, such as Lewy bodies, densely crosslinked intracellular protein deposits formed from neurofilament components and α-synuclein, have already been described in patients in advanced stages of the disease. There is, however, no indication of the involvement of AGE-induced crosslinking of α-synuclein in very early stages of the disease. In this study, we observed that AGEs and α-synuclein are similarly distributed in very early Lewy bodies in the human brain in cases with incidental Lewy body disease. These cases might be viewed as pre-Parkinson patients, i.e. patients who came for autopsy before the possible development of clinical signs of PD. AGEs are both markers of transition metal induced oxidative stress as well as, inducers of protein crosslinking and free radical formation by chemical and cellular processes. 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