Alteration of thioredoxin and glutaredoxin in the progression of Alzheimer's disease.
Identifieur interne : 000681 ( Main/Exploration ); précédent : 000680; suivant : 000682Alteration of thioredoxin and glutaredoxin in the progression of Alzheimer's disease.
Auteurs : Lisa Arodin [Suède] ; Heidrun Lamparter [Allemagne] ; H Kan Karlsson [Suède] ; Inger Nennesmo [Suède] ; Mikael Björnstedt [Suède] ; Johannes Schröder [Allemagne] ; Aristi P. Fernandes [Suède]Source :
- Journal of Alzheimer's disease : JAD [ 1875-8908 ] ; 2014.
Descripteurs français
- KwdFr :
- Adulte (MeSH), Adulte d'âge moyen (MeSH), Diagnostic précoce (MeSH), Femelle (MeSH), Glutarédoxines (), Hippocampe (anatomopathologie), Hippocampe (enzymologie), Hippocampe (métabolisme), Humains (MeSH), Maladie d'Alzheimer (), Maladie d'Alzheimer (diagnostic), Maladie d'Alzheimer (enzymologie), Marqueurs biologiques (), Mâle (MeSH), Sujet âgé (MeSH), Sujet âgé de 80 ans ou plus (MeSH), Thiorédoxines (), Évolution de la maladie (MeSH).
- MESH :
- anatomopathologie : Hippocampe.
- diagnostic : Maladie d'Alzheimer.
- enzymologie : Hippocampe, Maladie d'Alzheimer.
- métabolisme : Hippocampe.
- Adulte, Adulte d'âge moyen, Diagnostic précoce, Femelle, Glutarédoxines, Humains, Maladie d'Alzheimer, Marqueurs biologiques, Mâle, Sujet âgé, Sujet âgé de 80 ans ou plus, Thiorédoxines, Évolution de la maladie.
English descriptors
- KwdEn :
- Adult (MeSH), Aged (MeSH), Aged, 80 and over (MeSH), Alzheimer Disease (cerebrospinal fluid), Alzheimer Disease (diagnosis), Alzheimer Disease (enzymology), Biomarkers (cerebrospinal fluid), Disease Progression (MeSH), Early Diagnosis (MeSH), Female (MeSH), Glutaredoxins (cerebrospinal fluid), Hippocampus (enzymology), Hippocampus (metabolism), Hippocampus (pathology), Humans (MeSH), Male (MeSH), Middle Aged (MeSH), Thioredoxins (cerebrospinal fluid).
- MESH :
- chemical , cerebrospinal fluid : Biomarkers, Glutaredoxins, Thioredoxins.
- cerebrospinal fluid : Alzheimer Disease.
- diagnosis : Alzheimer Disease.
- enzymology : Alzheimer Disease, Hippocampus.
- metabolism : Hippocampus.
- pathology : Hippocampus.
- Adult, Aged, Aged, 80 and over, Disease Progression, Early Diagnosis, Female, Humans, Male, Middle Aged.
Abstract
Oxidative stress has an important role in the pathological process of most neurodegenerative disorders, including Alzheimer's disease (AD). The glutaredoxin (Grx) and thioredoxin (Trx) systems are central in maintaining a reduced environment in the cell and thus render protection against oxidative stress. Here, we show that Trx1 and Grx1 were released to the cerebrospinal fluid in 120 cases examined, and that the levels of these proteins increased significantly in the early stages of AD in comparison to mild cognitive impairment (MCI). Trx1 and Grx1 levels correlated with the established AD biomarkers tau and phospho-tau (p-tau). Moreover, by determining the levels of Trx1 and Grx1, discrimination between MCI converters and patients with stable MCI were possible. By applying the protein levels of Trx1 together with conventional diagnostic markers (Mini-Mental State Examination, tau, and p-tau) to a stepwise regression model, MCI stable, MCI converter, mild AD, and moderate AD was correctly diagnosed in 32 out of 33 cases. In order to further evaluate the involvement of these systems in AD, the immunoreactivity of Trx1, Trx2, Grx1, and Grx2 were investigated and the expression pattern was shown to be altered in hippocampus tissue sections from AD patients compared to controls. In conclusion, we introduce members of the thioredoxin super family of proteins as promising early biomarkers in the diagnosis of AD, suggesting their potential involvement in the pathogenesis of the disease.
DOI: 10.3233/JAD-131814
PubMed: 24270206
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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uniqKey="Lamparter H" first="Heidrun" last="Lamparter">Heidrun Lamparter</name><affiliation wicri:level="3"><nlm:affiliation>Section of Geriatric Psychiatry, University of Heidelberg, Heidelberg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Section of Geriatric Psychiatry, University of Heidelberg, Heidelberg</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author><author><name sortKey="Karlsson, H Kan" sort="Karlsson, H Kan" uniqKey="Karlsson H" first="H Kan" last="Karlsson">H Kan Karlsson</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Neuroscience, Karolinska Institutet, 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nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Karlsruhe</region><settlement type="city">Heidelberg</settlement></placeName></affiliation></author><author><name sortKey="Fernandes, Aristi P" sort="Fernandes, Aristi P" uniqKey="Fernandes A" first="Aristi P" last="Fernandes">Aristi P. Fernandes</name><affiliation wicri:level="3"><nlm:affiliation>Division of Pathology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Division of Pathology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm</wicri:regionArea><placeName><settlement type="city">Stockholm</settlement><region nuts="2">Svealand</region></placeName></affiliation></author></analytic><series><title level="j">Journal of Alzheimer's disease : JAD</title><idno type="eISSN">1875-8908</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult (MeSH)</term><term>Aged (MeSH)</term><term>Aged, 80 and over (MeSH)</term><term>Alzheimer Disease (cerebrospinal fluid)</term><term>Alzheimer Disease (diagnosis)</term><term>Alzheimer Disease (enzymology)</term><term>Biomarkers (cerebrospinal fluid)</term><term>Disease Progression (MeSH)</term><term>Early Diagnosis (MeSH)</term><term>Female (MeSH)</term><term>Glutaredoxins (cerebrospinal fluid)</term><term>Hippocampus (enzymology)</term><term>Hippocampus (metabolism)</term><term>Hippocampus (pathology)</term><term>Humans (MeSH)</term><term>Male (MeSH)</term><term>Middle Aged (MeSH)</term><term>Thioredoxins (cerebrospinal fluid)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adulte (MeSH)</term><term>Adulte d'âge moyen (MeSH)</term><term>Diagnostic précoce (MeSH)</term><term>Femelle (MeSH)</term><term>Glutarédoxines ()</term><term>Hippocampe (anatomopathologie)</term><term>Hippocampe (enzymologie)</term><term>Hippocampe (métabolisme)</term><term>Humains (MeSH)</term><term>Maladie d'Alzheimer ()</term><term>Maladie d'Alzheimer (diagnostic)</term><term>Maladie d'Alzheimer (enzymologie)</term><term>Marqueurs biologiques ()</term><term>Mâle (MeSH)</term><term>Sujet âgé (MeSH)</term><term>Sujet âgé de 80 ans ou plus (MeSH)</term><term>Thiorédoxines ()</term><term>Évolution de la maladie (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="cerebrospinal fluid" xml:lang="en"><term>Biomarkers</term><term>Glutaredoxins</term><term>Thioredoxins</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hippocampe</term></keywords><keywords scheme="MESH" qualifier="cerebrospinal fluid" xml:lang="en"><term>Alzheimer Disease</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Alzheimer Disease</term></keywords><keywords scheme="MESH" qualifier="diagnostic" xml:lang="fr"><term>Maladie d'Alzheimer</term></keywords><keywords scheme="MESH" qualifier="enzymologie" xml:lang="fr"><term>Hippocampe</term><term>Maladie d'Alzheimer</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Alzheimer Disease</term><term>Hippocampus</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hippocampus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Hippocampe</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hippocampus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Aged</term><term>Aged, 80 and over</term><term>Disease Progression</term><term>Early Diagnosis</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte</term><term>Adulte d'âge moyen</term><term>Diagnostic précoce</term><term>Femelle</term><term>Glutarédoxines</term><term>Humains</term><term>Maladie d'Alzheimer</term><term>Marqueurs biologiques</term><term>Mâle</term><term>Sujet âgé</term><term>Sujet âgé de 80 ans ou plus</term><term>Thiorédoxines</term><term>Évolution de la maladie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidative stress has an important role in the pathological process of most neurodegenerative disorders, including Alzheimer's disease (AD). The glutaredoxin (Grx) and thioredoxin (Trx) systems are central in maintaining a reduced environment in the cell and thus render protection against oxidative stress. Here, we show that Trx1 and Grx1 were released to the cerebrospinal fluid in 120 cases examined, and that the levels of these proteins increased significantly in the early stages of AD in comparison to mild cognitive impairment (MCI). Trx1 and Grx1 levels correlated with the established AD biomarkers tau and phospho-tau (p-tau). Moreover, by determining the levels of Trx1 and Grx1, discrimination between MCI converters and patients with stable MCI were possible. By applying the protein levels of Trx1 together with conventional diagnostic markers (Mini-Mental State Examination, tau, and p-tau) to a stepwise regression model, MCI stable, MCI converter, mild AD, and moderate AD was correctly diagnosed in 32 out of 33 cases. In order to further evaluate the involvement of these systems in AD, the immunoreactivity of Trx1, Trx2, Grx1, and Grx2 were investigated and the expression pattern was shown to be altered in hippocampus tissue sections from AD patients compared to controls. In conclusion, we introduce members of the thioredoxin super family of proteins as promising early biomarkers in the diagnosis of AD, suggesting their potential involvement in the pathogenesis of the disease.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">24270206</PMID><DateCompleted><Year>2014</Year><Month>10</Month><Day>30</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1875-8908</ISSN><JournalIssue CitedMedium="Internet"><Volume>39</Volume><Issue>4</Issue><PubDate><Year>2014</Year></PubDate></JournalIssue><Title>Journal of Alzheimer's disease : JAD</Title><ISOAbbreviation>J Alzheimers Dis</ISOAbbreviation></Journal><ArticleTitle>Alteration of thioredoxin and glutaredoxin in the progression of Alzheimer's disease.</ArticleTitle><Pagination><MedlinePgn>787-97</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.3233/JAD-131814</ELocationID><Abstract><AbstractText>Oxidative stress has an important role in the pathological process of most neurodegenerative disorders, including Alzheimer's disease (AD). The glutaredoxin (Grx) and thioredoxin (Trx) systems are central in maintaining a reduced environment in the cell and thus render protection against oxidative stress. Here, we show that Trx1 and Grx1 were released to the cerebrospinal fluid in 120 cases examined, and that the levels of these proteins increased significantly in the early stages of AD in comparison to mild cognitive impairment (MCI). Trx1 and Grx1 levels correlated with the established AD biomarkers tau and phospho-tau (p-tau). Moreover, by determining the levels of Trx1 and Grx1, discrimination between MCI converters and patients with stable MCI were possible. By applying the protein levels of Trx1 together with conventional diagnostic markers (Mini-Mental State Examination, tau, and p-tau) to a stepwise regression model, MCI stable, MCI converter, mild AD, and moderate AD was correctly diagnosed in 32 out of 33 cases. In order to further evaluate the involvement of these systems in AD, the immunoreactivity of Trx1, Trx2, Grx1, and Grx2 were investigated and the expression pattern was shown to be altered in hippocampus tissue sections from AD patients compared to controls. In conclusion, we introduce members of the thioredoxin super family of proteins as promising early biomarkers in the diagnosis of AD, suggesting their potential involvement in the pathogenesis of the disease.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Arodin</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Division of Pathology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lamparter</LastName><ForeName>Heidrun</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Section of Geriatric Psychiatry, University of Heidelberg, Heidelberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Karlsson</LastName><ForeName>Håkan</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nennesmo</LastName><ForeName>Inger</ForeName><Initials>I</Initials><AffiliationInfo><Affiliation>Division of Pathology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Björnstedt</LastName><ForeName>Mikael</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Division of Pathology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schröder</LastName><ForeName>Johannes</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>Section of Geriatric Psychiatry, University of Heidelberg, Heidelberg, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fernandes</LastName><ForeName>Aristi P</ForeName><Initials>AP</Initials><AffiliationInfo><Affiliation>Division of Pathology, Department of Laboratory Medicine, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>J Alzheimers Dis</MedlineTA><NlmUniqueID>9814863</NlmUniqueID><ISSNLinking>1387-2877</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015415">Biomarkers</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C516005">GLRX protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D054477">Glutaredoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C491203">TXN protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>52500-60-4</RegistryNumber><NameOfSubstance UI="D013879">Thioredoxins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000328" MajorTopicYN="N">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000369" MajorTopicYN="N">Aged, 80 and over</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000544" MajorTopicYN="N">Alzheimer Disease</DescriptorName><QualifierName UI="Q000134" MajorTopicYN="Y">cerebrospinal fluid</QualifierName><QualifierName UI="Q000175" MajorTopicYN="Y">diagnosis</QualifierName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015415" MajorTopicYN="N">Biomarkers</DescriptorName><QualifierName UI="Q000134" MajorTopicYN="N">cerebrospinal fluid</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="Y">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D042241" MajorTopicYN="N">Early Diagnosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName><QualifierName UI="Q000134" MajorTopicYN="Y">cerebrospinal fluid</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006624" MajorTopicYN="N">Hippocampus</DescriptorName><QualifierName UI="Q000201" MajorTopicYN="N">enzymology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013879" MajorTopicYN="N">Thioredoxins</DescriptorName><QualifierName UI="Q000134" MajorTopicYN="Y">cerebrospinal fluid</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Alzheimer's disease</Keyword><Keyword MajorTopicYN="N">glutaredoxin</Keyword><Keyword MajorTopicYN="N">mild cognitive impairment</Keyword><Keyword MajorTopicYN="N">thioredoxin</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year><Month>11</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2013</Year><Month>11</Month><Day>26</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2014</Year><Month>10</Month><Day>31</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">24270206</ArticleId><ArticleId IdType="pii">28881K8M04264J7W</ArticleId><ArticleId IdType="doi">10.3233/JAD-131814</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li><li>Suède</li></country><region><li>Bade-Wurtemberg</li><li>District de Karlsruhe</li><li>Svealand</li></region><settlement><li>Heidelberg</li><li>Stockholm</li></settlement></list><tree><country name="Suède"><region name="Svealand"><name sortKey="Arodin, Lisa" sort="Arodin, Lisa" uniqKey="Arodin L" first="Lisa" last="Arodin">Lisa Arodin</name></region><name sortKey="Bjornstedt, Mikael" sort="Bjornstedt, Mikael" uniqKey="Bjornstedt M" first="Mikael" last="Björnstedt">Mikael Björnstedt</name><name sortKey="Fernandes, Aristi P" sort="Fernandes, Aristi P" uniqKey="Fernandes A" first="Aristi P" last="Fernandes">Aristi P. Fernandes</name><name sortKey="Karlsson, H Kan" sort="Karlsson, H Kan" uniqKey="Karlsson H" first="H Kan" last="Karlsson">H Kan Karlsson</name><name sortKey="Nennesmo, Inger" sort="Nennesmo, Inger" uniqKey="Nennesmo I" first="Inger" last="Nennesmo">Inger Nennesmo</name></country><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Lamparter, Heidrun" sort="Lamparter, Heidrun" uniqKey="Lamparter H" first="Heidrun" last="Lamparter">Heidrun Lamparter</name></region><name sortKey="Schroder, Johannes" sort="Schroder, Johannes" uniqKey="Schroder J" first="Johannes" last="Schröder">Johannes Schröder</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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