Changes in Tryptophan Catabolite (TRYCAT) Pathway Patterning Are Associated with Mild Impairments in Declarative Memory in Schizophrenia and Deficits in Semantic and Episodic Memory Coupled with Increased False-Memory Creation in Deficit Schizophrenia.
Identifieur interne : 001034 ( PubMed/Checkpoint ); précédent : 001033; suivant : 001035Changes in Tryptophan Catabolite (TRYCAT) Pathway Patterning Are Associated with Mild Impairments in Declarative Memory in Schizophrenia and Deficits in Semantic and Episodic Memory Coupled with Increased False-Memory Creation in Deficit Schizophrenia.
Auteurs : Buranee Kanchanatawan [Thaïlande] ; Solaphat Hemrungrojn [Thaïlande] ; Supaksorn Thika [Thaïlande] ; Sunee Sirivichayakul [Thaïlande] ; Kiat Ruxrungtham [Thaïlande] ; André F. Carvalho [Brésil] ; Michel Geffard [France] ; George Anderson [Royaume-Uni] ; Michael Maes [Thaïlande]Source :
- Molecular neurobiology [ 1559-1182 ] ; 2017.
Abstract
Evidence indicates that schizophrenia and in particular negative symptoms and deficit schizophrenia are accompanied by neurocognitive impairments and changes in the patterning of the tryptophan catabolite (TRYCAT) pathway. This cross-sectional study was carried out to examine the associations between cognitive functions (as measured with Consortium to Establish a Registry for Alzheimer's disease (CERAD)) and TRYCAT pathway patterning in patients with (n = 40) and without (n = 40) deficit schizophrenia and normal controls (n = 40). Cognitive measures were assessed with the Verbal Fluency Test (VFT), Boston Naming Test (BNT), Mini-Mental State Examination (MMSE), Word List Memory (WLM), Constructional Praxis, Word List Recall (WLRecall), and Word List Recognition (WLRecognition), while TRYCAT measurements assessed the IgA/IgM responses to noxious TRYCATs, namely quinolinic acid (QA), 3-OH-kynurenine (3HK), picolinic acid (PA), and xanthurenic (XA) acid, and more protective (PRO) TRYCATs, including kynurenic acid (KA) and anthranilic acid (AA). IgA NOX/PRO, IgM KA/3HK, and IgA/IgM NOX/PRO ratios were computed. Schizophrenia was accompanied by lower VFT and WLM, while BNT (dysnomia) and MMSE are significantly lower in multiple- than first-episode schizophrenia. Deficit schizophrenia is strongly associated with worse outcomes on VFT, MMSE, WLM, WLRecall, WLRecognition, and delayed recall savings and increased false memories. Around 40-50% of the variance in negative symptoms' scores was explained by VFT, WLM, WLRecall, and MMSE. Increases in IgA NOX/PRO, IgM KA/3HK, and/or IgA/IgM NOX/PRO ratios were associated with impairments in VFT, BNT, MMSE, WLM, WLRecall, WLRecognition, and false-memory creation. In conclusion, nondeficit schizophrenia is accompanied by mild memory impairments, while disease progression is accompanied by broader cognitive impairments. Deficit schizophrenia and negative symptoms are strongly associated with deficits in working memory, delayed recall and recognition, and increased false-memory creation. These cognitive impairments and memory deficits are in part explained by increased production and/or attenuated regulation of TRYCATs with neurotoxic, excitotoxic, immune-inflammatory, oxidative, and nitrosative potential, which may contribute to neuroprogression.
DOI: 10.1007/s12035-017-0751-8
PubMed: 28875464
Affiliations:
- Brésil, France, Royaume-Uni, Thaïlande
- Angleterre, Aquitaine, Aquitaine-Limousin-Poitou-Charentes, Ceará, Grand Londres
- Bordeaux, Londres, Talence
- Université fédérale du Ceará
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Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea><wicri:noRegion>Bangkok</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28875464</idno><idno type="pmid">28875464</idno><idno type="doi">10.1007/s12035-017-0751-8</idno><idno type="wicri:Area/PubMed/Corpus">000510</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000510</idno><idno type="wicri:Area/PubMed/Curation">000508</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000508</idno><idno type="wicri:Area/PubMed/Checkpoint">000508</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" 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uniqKey="Hemrungrojn S" first="Solaphat" last="Hemrungrojn">Solaphat Hemrungrojn</name><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea><wicri:noRegion>Bangkok</wicri:noRegion></affiliation></author><author><name sortKey="Thika, Supaksorn" sort="Thika, Supaksorn" uniqKey="Thika S" first="Supaksorn" last="Thika">Supaksorn Thika</name><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea><wicri:noRegion>Bangkok</wicri:noRegion></affiliation></author><author><name sortKey="Sirivichayakul, Sunee" sort="Sirivichayakul, Sunee" uniqKey="Sirivichayakul S" first="Sunee" last="Sirivichayakul">Sunee Sirivichayakul</name><affiliation wicri:level="1"><nlm:affiliation>Division of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Division of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330</wicri:regionArea><wicri:noRegion>10330</wicri:noRegion></affiliation></author><author><name sortKey="Ruxrungtham, Kiat" sort="Ruxrungtham, Kiat" uniqKey="Ruxrungtham K" first="Kiat" last="Ruxrungtham">Kiat Ruxrungtham</name><affiliation wicri:level="1"><nlm:affiliation>Division of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Division of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330</wicri:regionArea><wicri:noRegion>10330</wicri:noRegion></affiliation></author><author><name sortKey="Carvalho, Andre F" sort="Carvalho, Andre F" uniqKey="Carvalho A" first="André F" last="Carvalho">André F. Carvalho</name><affiliation wicri:level="4"><nlm:affiliation>Department of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.</nlm:affiliation><country xml:lang="fr">Brésil</country><wicri:regionArea>Department of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE</wicri:regionArea><placeName><region type="state">Ceará</region></placeName><orgName type="university">Université fédérale du Ceará</orgName></affiliation></author><author><name sortKey="Geffard, Michel" sort="Geffard, Michel" uniqKey="Geffard M" first="Michel" last="Geffard">Michel Geffard</name><affiliation wicri:level="3"><nlm:affiliation>Research Department, IDRPHT, Talence, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Research Department, IDRPHT, Talence</wicri:regionArea><placeName><region type="region" nuts="2">Aquitaine-Limousin-Poitou-Charentes</region><region type="old region" nuts="2">Aquitaine</region><settlement type="city">Talence</settlement><settlement type="city" wicri:auto="agglo">Bordeaux</settlement></placeName></affiliation></author><author><name sortKey="Anderson, George" sort="Anderson, George" uniqKey="Anderson G" first="George" last="Anderson">George Anderson</name><affiliation wicri:level="3"><nlm:affiliation>CRC Scotland & London, Eccleston Square, London, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>CRC Scotland & London, Eccleston Square, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Maes, Michael" sort="Maes, Michael" uniqKey="Maes M" first="Michael" last="Maes">Michael Maes</name><affiliation wicri:level="1"><nlm:affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.</nlm:affiliation><country xml:lang="fr">Thaïlande</country><wicri:regionArea>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok</wicri:regionArea><wicri:noRegion>Bangkok</wicri:noRegion></affiliation></author></analytic><series><title level="j">Molecular neurobiology</title><idno type="eISSN">1559-1182</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Evidence indicates that schizophrenia and in particular negative symptoms and deficit schizophrenia are accompanied by neurocognitive impairments and changes in the patterning of the tryptophan catabolite (TRYCAT) pathway. This cross-sectional study was carried out to examine the associations between cognitive functions (as measured with Consortium to Establish a Registry for Alzheimer's disease (CERAD)) and TRYCAT pathway patterning in patients with (n = 40) and without (n = 40) deficit schizophrenia and normal controls (n = 40). Cognitive measures were assessed with the Verbal Fluency Test (VFT), Boston Naming Test (BNT), Mini-Mental State Examination (MMSE), Word List Memory (WLM), Constructional Praxis, Word List Recall (WLRecall), and Word List Recognition (WLRecognition), while TRYCAT measurements assessed the IgA/IgM responses to noxious TRYCATs, namely quinolinic acid (QA), 3-OH-kynurenine (3HK), picolinic acid (PA), and xanthurenic (XA) acid, and more protective (PRO) TRYCATs, including kynurenic acid (KA) and anthranilic acid (AA). IgA NOX/PRO, IgM KA/3HK, and IgA/IgM NOX/PRO ratios were computed. Schizophrenia was accompanied by lower VFT and WLM, while BNT (dysnomia) and MMSE are significantly lower in multiple- than first-episode schizophrenia. Deficit schizophrenia is strongly associated with worse outcomes on VFT, MMSE, WLM, WLRecall, WLRecognition, and delayed recall savings and increased false memories. Around 40-50% of the variance in negative symptoms' scores was explained by VFT, WLM, WLRecall, and MMSE. Increases in IgA NOX/PRO, IgM KA/3HK, and/or IgA/IgM NOX/PRO ratios were associated with impairments in VFT, BNT, MMSE, WLM, WLRecall, WLRecognition, and false-memory creation. In conclusion, nondeficit schizophrenia is accompanied by mild memory impairments, while disease progression is accompanied by broader cognitive impairments. Deficit schizophrenia and negative symptoms are strongly associated with deficits in working memory, delayed recall and recognition, and increased false-memory creation. These cognitive impairments and memory deficits are in part explained by increased production and/or attenuated regulation of TRYCATs with neurotoxic, excitotoxic, immune-inflammatory, oxidative, and nitrosative potential, which may contribute to neuroprogression.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">28875464</PMID><DateCreated><Year>2017</Year><Month>09</Month><Day>06</Day></DateCreated><DateRevised><Year>2017</Year><Month>09</Month><Day>06</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1559-1182</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2017</Year><Month>Sep</Month><Day>05</Day></PubDate></JournalIssue><Title>Molecular neurobiology</Title><ISOAbbreviation>Mol. Neurobiol.</ISOAbbreviation></Journal><ArticleTitle>Changes in Tryptophan Catabolite (TRYCAT) Pathway Patterning Are Associated with Mild Impairments in Declarative Memory in Schizophrenia and Deficits in Semantic and Episodic Memory Coupled with Increased False-Memory Creation in Deficit Schizophrenia.</ArticleTitle><ELocationID EIdType="doi" ValidYN="Y">10.1007/s12035-017-0751-8</ELocationID><Abstract><AbstractText>Evidence indicates that schizophrenia and in particular negative symptoms and deficit schizophrenia are accompanied by neurocognitive impairments and changes in the patterning of the tryptophan catabolite (TRYCAT) pathway. This cross-sectional study was carried out to examine the associations between cognitive functions (as measured with Consortium to Establish a Registry for Alzheimer's disease (CERAD)) and TRYCAT pathway patterning in patients with (n = 40) and without (n = 40) deficit schizophrenia and normal controls (n = 40). Cognitive measures were assessed with the Verbal Fluency Test (VFT), Boston Naming Test (BNT), Mini-Mental State Examination (MMSE), Word List Memory (WLM), Constructional Praxis, Word List Recall (WLRecall), and Word List Recognition (WLRecognition), while TRYCAT measurements assessed the IgA/IgM responses to noxious TRYCATs, namely quinolinic acid (QA), 3-OH-kynurenine (3HK), picolinic acid (PA), and xanthurenic (XA) acid, and more protective (PRO) TRYCATs, including kynurenic acid (KA) and anthranilic acid (AA). IgA NOX/PRO, IgM KA/3HK, and IgA/IgM NOX/PRO ratios were computed. Schizophrenia was accompanied by lower VFT and WLM, while BNT (dysnomia) and MMSE are significantly lower in multiple- than first-episode schizophrenia. Deficit schizophrenia is strongly associated with worse outcomes on VFT, MMSE, WLM, WLRecall, WLRecognition, and delayed recall savings and increased false memories. Around 40-50% of the variance in negative symptoms' scores was explained by VFT, WLM, WLRecall, and MMSE. Increases in IgA NOX/PRO, IgM KA/3HK, and/or IgA/IgM NOX/PRO ratios were associated with impairments in VFT, BNT, MMSE, WLM, WLRecall, WLRecognition, and false-memory creation. In conclusion, nondeficit schizophrenia is accompanied by mild memory impairments, while disease progression is accompanied by broader cognitive impairments. Deficit schizophrenia and negative symptoms are strongly associated with deficits in working memory, delayed recall and recognition, and increased false-memory creation. These cognitive impairments and memory deficits are in part explained by increased production and/or attenuated regulation of TRYCATs with neurotoxic, excitotoxic, immune-inflammatory, oxidative, and nitrosative potential, which may contribute to neuroprogression.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kanchanatawan</LastName><ForeName>Buranee</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Hemrungrojn</LastName><ForeName>Solaphat</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Thika</LastName><ForeName>Supaksorn</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sirivichayakul</LastName><ForeName>Sunee</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Division of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ruxrungtham</LastName><ForeName>Kiat</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Division of Allergy and Clinical Immunology, Department of Medicine, Faculty of Medicine, Chulalongkorn University, Bangkok, 10330, Thailand.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Carvalho</LastName><ForeName>André F</ForeName><Initials>AF</Initials><AffiliationInfo><Affiliation>Department of Clinical Medicine and Translational Psychiatry Research Group, Faculty of Medicine, Federal University of Ceará, Fortaleza, CE, Brazil.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Geffard</LastName><ForeName>Michel</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Research Department, IDRPHT, Talence, France.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>GEMAC, Saint Jean d'Illac, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Anderson</LastName><ForeName>George</ForeName><Initials>G</Initials><AffiliationInfo><Affiliation>CRC Scotland & London, Eccleston Square, London, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Maes</LastName><ForeName>Michael</ForeName><Initials>M</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-2012-871X</Identifier><AffiliationInfo><Affiliation>Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>IMPACT Strategic Research Center, Deakin University, Geelong, Australia. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Revitalis, Waalre, the Netherlands. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Department of Psychiatry, Medical University of Plovdiv, Plovdiv, Bulgaria. dr.michaelmaes@hotmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>09</Month><Day>05</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mol Neurobiol</MedlineTA><NlmUniqueID>8900963</NlmUniqueID><ISSNLinking>0893-7648</ISSNLinking></MedlineJournalInfo><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Compensatory anti-inflammatory reflex system</Keyword><Keyword MajorTopicYN="N">Cytokines</Keyword><Keyword MajorTopicYN="N">Immune activation</Keyword><Keyword MajorTopicYN="N">Inflammation</Keyword><Keyword MajorTopicYN="N">Schizophrenia</Keyword><Keyword MajorTopicYN="N">Tryptophan</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2017</Year><Month>04</Month><Day>29</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2017</Year><Month>08</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2017</Year><Month>9</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2017</Year><Month>9</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2017</Year><Month>9</Month><Day>7</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">28875464</ArticleId><ArticleId IdType="doi">10.1007/s12035-017-0751-8</ArticleId><ArticleId IdType="pii">10.1007/s12035-017-0751-8</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Brésil</li><li>France</li><li>Royaume-Uni</li><li>Thaïlande</li></country><region><li>Angleterre</li><li>Aquitaine</li><li>Aquitaine-Limousin-Poitou-Charentes</li><li>Ceará</li><li>Grand Londres</li></region><settlement><li>Bordeaux</li><li>Londres</li><li>Talence</li></settlement><orgName><li>Université fédérale du Ceará</li></orgName></list><tree><country name="Thaïlande"><noRegion><name sortKey="Kanchanatawan, Buranee" sort="Kanchanatawan, Buranee" uniqKey="Kanchanatawan B" first="Buranee" last="Kanchanatawan">Buranee Kanchanatawan</name></noRegion><name sortKey="Hemrungrojn, Solaphat" sort="Hemrungrojn, Solaphat" uniqKey="Hemrungrojn S" first="Solaphat" last="Hemrungrojn">Solaphat Hemrungrojn</name><name sortKey="Maes, Michael" sort="Maes, Michael" uniqKey="Maes M" first="Michael" last="Maes">Michael Maes</name><name sortKey="Ruxrungtham, Kiat" sort="Ruxrungtham, Kiat" uniqKey="Ruxrungtham K" first="Kiat" last="Ruxrungtham">Kiat Ruxrungtham</name><name sortKey="Sirivichayakul, Sunee" sort="Sirivichayakul, Sunee" uniqKey="Sirivichayakul S" first="Sunee" last="Sirivichayakul">Sunee Sirivichayakul</name><name sortKey="Thika, Supaksorn" sort="Thika, Supaksorn" uniqKey="Thika S" first="Supaksorn" last="Thika">Supaksorn Thika</name></country><country name="Brésil"><region name="Ceará"><name sortKey="Carvalho, Andre F" sort="Carvalho, Andre F" uniqKey="Carvalho A" first="André F" last="Carvalho">André F. Carvalho</name></region></country><country name="France"><region name="Aquitaine-Limousin-Poitou-Charentes"><name sortKey="Geffard, Michel" sort="Geffard, Michel" uniqKey="Geffard M" first="Michel" last="Geffard">Michel Geffard</name></region></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Anderson, George" sort="Anderson, George" uniqKey="Anderson G" first="George" last="Anderson">George Anderson</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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