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Increased oxidation of certain glycolysis and energy metabolism enzymes in the frontal cortex in Lewy body diseases

Identifieur interne : 000876 ( Main/Corpus ); précédent : 000875; suivant : 000877

Increased oxidation of certain glycolysis and energy metabolism enzymes in the frontal cortex in Lewy body diseases

Auteurs : Anna G Mez ; Isidre Ferrer

Source :

RBID : ISTEX:79BE575F395582EA66DB754DF62D5361C2F9BBD8

English descriptors

Abstract

Lipoxidative damage of aldolase A, enolase 1, and glyceraldehyde dehydrogenase (GAPDH) was found in the frontal cortex in a percentage of aged controls by bidimensional gel electrophoresis, Western blot test, in‐gel digestion, and mass spectrometry. Aldolase A and enolase 1 were altered in 12 of 19 cases, whereas oxidation of GAPDH was found in 6 of 19 controls. The three enzymes were oxidized in the frontal cortex in the majority of cases of incidental Parkinson's disease (iPD), PD, and dementia with Lewy bodies (DLB). Differences were statistically significant (χ2 test) for GAPDH in PD and DLB. Densitometric studies have shown that the ratio of oxidized protein per spot is higher in iPD, PD, and DLB compared with controls. These findings show oxidation of three enzymes linked with glycolysis and energy metabolism in the adult human brain as well as increased oxidation of aldolase A, enolase 1, and GAPDH in the frontal cortex in Lewy body diseases. Modifications of these enzymes may result in decreased activity and may partly account for impaired metabolism and function of the frontal lobe in PD. © 2008 Wiley‐Liss, Inc.

Url:
DOI: 10.1002/jnr.21904

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ISTEX:79BE575F395582EA66DB754DF62D5361C2F9BBD8

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<namePart type="given">Isidre</namePart>
<namePart type="family">Ferrer</namePart>
<affiliation>Institut Neuropatologia, Servei Anatomia Patològica, Idibell‐Hospital Universitari de Bellvitge, Hospitalet de Llobregat, Spain</affiliation>
<description>Correspondence: Institut Neuropatologia, Servei Anatomia Patològica, Idibell‐Hospital Universitari de Bellvitge, carrer Feixa Llarga sn 08907, Hospitalet de Llobregat, Spain</description>
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<place>
<placeTerm type="text">Hoboken</placeTerm>
</place>
<dateIssued encoding="w3cdtf">2009-03</dateIssued>
<dateCaptured encoding="w3cdtf">2008-06-04</dateCaptured>
<dateValid encoding="w3cdtf">2008-08-19</dateValid>
<copyrightDate encoding="w3cdtf">2009</copyrightDate>
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<languageTerm type="code" authority="rfc3066">en</languageTerm>
<languageTerm type="code" authority="iso639-2b">eng</languageTerm>
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<abstract lang="en">Lipoxidative damage of aldolase A, enolase 1, and glyceraldehyde dehydrogenase (GAPDH) was found in the frontal cortex in a percentage of aged controls by bidimensional gel electrophoresis, Western blot test, in‐gel digestion, and mass spectrometry. Aldolase A and enolase 1 were altered in 12 of 19 cases, whereas oxidation of GAPDH was found in 6 of 19 controls. The three enzymes were oxidized in the frontal cortex in the majority of cases of incidental Parkinson's disease (iPD), PD, and dementia with Lewy bodies (DLB). Differences were statistically significant (χ2 test) for GAPDH in PD and DLB. Densitometric studies have shown that the ratio of oxidized protein per spot is higher in iPD, PD, and DLB compared with controls. These findings show oxidation of three enzymes linked with glycolysis and energy metabolism in the adult human brain as well as increased oxidation of aldolase A, enolase 1, and GAPDH in the frontal cortex in Lewy body diseases. Modifications of these enzymes may result in decreased activity and may partly account for impaired metabolism and function of the frontal lobe in PD. © 2008 Wiley‐Liss, Inc.</abstract>
<note type="funding">Spanish Ministry of Health - No. PI05/1570; </note>
<note type="funding">Instituto de Salud Carlos III</note>
<note type="funding">European Commission under the Sixth Framework Programme</note>
<note type="funding">BrainNet Europe II - No. LSHM‐CT‐2004‐503039; </note>
<note type="funding">INDABIP</note>
<subject lang="en">
<genre>Keywords</genre>
<topic>Parkinson disease</topic>
<topic>Lewy body disease</topic>
<topic>dementia with Lewy bodies</topic>
<topic>incidental Lewy body disease</topic>
<topic>aldolase A</topic>
<topic>enolase 1</topic>
<topic>glyceraldehyde dehydrogenase</topic>
<topic>oxidative damage</topic>
</subject>
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<title>Journal of Neuroscience Research</title>
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<titleInfo type="abbreviated">
<title>J. Neurosci. Res.</title>
</titleInfo>
<genre type="Journal">journal</genre>
<subject>
<genre>article category</genre>
<topic>Research Article</topic>
</subject>
<identifier type="ISSN">0360-4012</identifier>
<identifier type="eISSN">1097-4547</identifier>
<identifier type="DOI">10.1002/(ISSN)1097-4547</identifier>
<identifier type="PublisherID">JNR</identifier>
<part>
<date>2009</date>
<detail type="volume">
<caption>vol.</caption>
<number>87</number>
</detail>
<detail type="issue">
<caption>no.</caption>
<number>4</number>
</detail>
<extent unit="pages">
<start>1002</start>
<end>1013</end>
<total>12</total>
</extent>
</part>
</relatedItem>
<identifier type="istex">79BE575F395582EA66DB754DF62D5361C2F9BBD8</identifier>
<identifier type="DOI">10.1002/jnr.21904</identifier>
<identifier type="ArticleID">JNR21904</identifier>
<accessCondition type="use and reproduction" contentType="copyright">Copyright © 2008 Wiley‐Liss, Inc.</accessCondition>
<recordInfo>
<recordContentSource>WILEY</recordContentSource>
<recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin>
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</mods>
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<serie></serie>
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</record>

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