Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: a Nomothetic Network Psychiatry Approach
There is now evidence that schizophrenia and deficit schizophrenia are neuro-immune conditions and that oxidative stress toxicity (OSTOX) may play a pathophysiological role. Aims of the study: to compare OSTOX biomarkers and antioxidant (ANTIOX) defenses in deficit versus non-deficit schizophrenia....
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| Veröffentlicht in: | Molecular neurobiology 2020-11, Vol.57 (11), p.4578-4597 |
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| creator | Maes, Michael Sirivichayakul, Sunee Matsumoto, Andressa Keiko Michelin, Ana Paula de Oliveira Semeão, Laura de Lima Pedrão, João Victor Moreira, Estefania G. Barbosa, Decio S. Carvalho, Andre F. Solmi, Marco Kanchanatawan, Buranee |
| description | There is now evidence that schizophrenia and deficit schizophrenia are neuro-immune conditions and that oxidative stress toxicity (OSTOX) may play a pathophysiological role. Aims of the study: to compare OSTOX biomarkers and antioxidant (ANTIOX) defenses in deficit versus non-deficit schizophrenia. We examined lipid hydroperoxides (LOOH), malondialdehyde (MDA), advanced oxidation protein products (AOPP), sulfhydryl (–SH) groups, paraoxonase 1 (PON1) activity and PON1 Q192R genotypes, and total radical-trapping antioxidant parameter (TRAP) as well as immune biomarkers in patients with deficit (
n
= 40) and non-deficit (
n
= 40) schizophrenia and healthy controls (
n
= 40). Deficit schizophrenia is characterized by significantly increased levels of AOPP and lowered –SH, and PON1 activity, while no changes in the OSTOX/ANTIOX biomarkers were found in non-deficit schizophrenia. An increased OSTOX/ANTIOX ratio was significantly associated with deficit versus non-deficit schizophrenia (odds ratio = 3.15,
p
|
| doi_str_mv | 10.1007/s12035-020-02047-5 |
| format | Article |
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n
= 40) and non-deficit (
n
= 40) schizophrenia and healthy controls (
n
= 40). Deficit schizophrenia is characterized by significantly increased levels of AOPP and lowered –SH, and PON1 activity, while no changes in the OSTOX/ANTIOX biomarkers were found in non-deficit schizophrenia. An increased OSTOX/ANTIOX ratio was significantly associated with deficit versus non-deficit schizophrenia (odds ratio = 3.15,
p
< 0.001). Partial least squares analysis showed that 47.6% of the variance in a latent vector extracted from psychosis, excitation, hostility, mannerism, negative symptoms, psychomotor retardation, formal thought disorders, and neurocognitive test scores was explained by LOOH+AOPP, PON1 genotype + activity, CCL11, tumor necrosis factor (TNF)-α, and IgA responses to neurotoxic tryptophan catabolites (TRYCATs), whereas –SH groups and IgM responses to MDA showed indirect effects mediated by OSTOX and neuro-immune biomarkers. When overall severity of schizophrenia increases, multiple immune and oxidative (especially protein oxidation indicating chlorinative stress) neurotoxicities and impairments in immune-protective resilience become more prominent and shape a distinct nosological entity, namely deficit schizophrenia. The nomothetic network psychiatry approach allows building causal-pathway-phenotype models using machine learning techniques.</description><identifier>ISSN: 0893-7648</identifier><identifier>EISSN: 1559-1182</identifier><identifier>DOI: 10.1007/s12035-020-02047-5</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Antioxidants ; Biomarkers ; Biomedical and Life Sciences ; Biomedicine ; Catabolites ; Cell Biology ; Cognition ; Emotional behavior ; Genotypes ; Immunoglobulin A ; Immunoglobulin M ; Intellectual disabilities ; Lipid peroxidation ; Mental disorders ; Neurobiology ; Neurology ; Neurosciences ; Neurotoxicity ; Original Article ; Oxidative stress ; Paraoxonase ; Paraoxonase 1 ; Phenotypes ; Psychosis ; Schizophrenia ; Tryptophan ; Tumor necrosis factor-TNF</subject><ispartof>Molecular neurobiology, 2020-11, Vol.57 (11), p.4578-4597</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c352t-8e30d558d025fc11e5376965f6de490511b12ff1969bf5a03d348db0a5ab46313</citedby><cites>FETCH-LOGICAL-c352t-8e30d558d025fc11e5376965f6de490511b12ff1969bf5a03d348db0a5ab46313</cites><orcidid>0000-0002-2012-871X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12035-020-02047-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12035-020-02047-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids></links><search><creatorcontrib>Maes, Michael</creatorcontrib><creatorcontrib>Sirivichayakul, Sunee</creatorcontrib><creatorcontrib>Matsumoto, Andressa Keiko</creatorcontrib><creatorcontrib>Michelin, Ana Paula</creatorcontrib><creatorcontrib>de Oliveira Semeão, Laura</creatorcontrib><creatorcontrib>de Lima Pedrão, João Victor</creatorcontrib><creatorcontrib>Moreira, Estefania G.</creatorcontrib><creatorcontrib>Barbosa, Decio S.</creatorcontrib><creatorcontrib>Carvalho, Andre F.</creatorcontrib><creatorcontrib>Solmi, Marco</creatorcontrib><creatorcontrib>Kanchanatawan, Buranee</creatorcontrib><title>Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: a Nomothetic Network Psychiatry Approach</title><title>Molecular neurobiology</title><addtitle>Mol Neurobiol</addtitle><description>There is now evidence that schizophrenia and deficit schizophrenia are neuro-immune conditions and that oxidative stress toxicity (OSTOX) may play a pathophysiological role. Aims of the study: to compare OSTOX biomarkers and antioxidant (ANTIOX) defenses in deficit versus non-deficit schizophrenia. We examined lipid hydroperoxides (LOOH), malondialdehyde (MDA), advanced oxidation protein products (AOPP), sulfhydryl (–SH) groups, paraoxonase 1 (PON1) activity and PON1 Q192R genotypes, and total radical-trapping antioxidant parameter (TRAP) as well as immune biomarkers in patients with deficit (
n
= 40) and non-deficit (
n
= 40) schizophrenia and healthy controls (
n
= 40). Deficit schizophrenia is characterized by significantly increased levels of AOPP and lowered –SH, and PON1 activity, while no changes in the OSTOX/ANTIOX biomarkers were found in non-deficit schizophrenia. An increased OSTOX/ANTIOX ratio was significantly associated with deficit versus non-deficit schizophrenia (odds ratio = 3.15,
p
< 0.001). Partial least squares analysis showed that 47.6% of the variance in a latent vector extracted from psychosis, excitation, hostility, mannerism, negative symptoms, psychomotor retardation, formal thought disorders, and neurocognitive test scores was explained by LOOH+AOPP, PON1 genotype + activity, CCL11, tumor necrosis factor (TNF)-α, and IgA responses to neurotoxic tryptophan catabolites (TRYCATs), whereas –SH groups and IgM responses to MDA showed indirect effects mediated by OSTOX and neuro-immune biomarkers. When overall severity of schizophrenia increases, multiple immune and oxidative (especially protein oxidation indicating chlorinative stress) neurotoxicities and impairments in immune-protective resilience become more prominent and shape a distinct nosological entity, namely deficit schizophrenia. The nomothetic network psychiatry approach allows building causal-pathway-phenotype models using machine learning techniques.</description><subject>Antioxidants</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Catabolites</subject><subject>Cell Biology</subject><subject>Cognition</subject><subject>Emotional behavior</subject><subject>Genotypes</subject><subject>Immunoglobulin A</subject><subject>Immunoglobulin M</subject><subject>Intellectual disabilities</subject><subject>Lipid peroxidation</subject><subject>Mental disorders</subject><subject>Neurobiology</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Neurotoxicity</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Paraoxonase</subject><subject>Paraoxonase 1</subject><subject>Phenotypes</subject><subject>Psychosis</subject><subject>Schizophrenia</subject><subject>Tryptophan</subject><subject>Tumor necrosis factor-TNF</subject><issn>0893-7648</issn><issn>1559-1182</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kMtOwzAQRS0EEuXxA6wssQ6M7TgPdhVvqQIkYG25yZiGtnGwXUr5CL4ZhyCxYzGaxZx7r-YScsTghAHkp55xEDIBDv2keSK3yIhJWSaMFXybjKAoRZJnabFL9rx_BeCcQT4iXxO7Roc1HbehsR9NrdtAL9Bg69FT3db0tq0cah-R-_4cmnekT5GsmrChY4f0Ri8WS-3mnlrTS_sLfaxmzaftZg7bRp9RTe_s0oYZhqaidxjW1s3pg99ESgcXfbrOWV3NDsiO0QuPh797nzxfXT6d3yST--vb8_EkqYTkISlQQC1lUQOXpmIMpcizMpMmqzEtQTI2ZdwYVmbl1EgNohZpUU9BSz1NM8HEPjkefGPs2wp9UK925doYqXghgBVZLiBSfKAqZ713aFTnmvjqRjFQfe9q6F3FztVP70pGkRhEPsLtC7o_639U3yODh1E</recordid><startdate>20201101</startdate><enddate>20201101</enddate><creator>Maes, Michael</creator><creator>Sirivichayakul, Sunee</creator><creator>Matsumoto, Andressa 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Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: a Nomothetic Network Psychiatry Approach</title><author>Maes, Michael ; Sirivichayakul, Sunee ; Matsumoto, Andressa Keiko ; Michelin, Ana Paula ; de Oliveira Semeão, Laura ; de Lima Pedrão, João Victor ; Moreira, Estefania G. ; Barbosa, Decio S. ; Carvalho, Andre F. ; Solmi, Marco ; Kanchanatawan, Buranee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c352t-8e30d558d025fc11e5376965f6de490511b12ff1969bf5a03d348db0a5ab46313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Antioxidants</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Catabolites</topic><topic>Cell Biology</topic><topic>Cognition</topic><topic>Emotional behavior</topic><topic>Genotypes</topic><topic>Immunoglobulin A</topic><topic>Immunoglobulin M</topic><topic>Intellectual disabilities</topic><topic>Lipid peroxidation</topic><topic>Mental disorders</topic><topic>Neurobiology</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Neurotoxicity</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Paraoxonase</topic><topic>Paraoxonase 1</topic><topic>Phenotypes</topic><topic>Psychosis</topic><topic>Schizophrenia</topic><topic>Tryptophan</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Maes, Michael</creatorcontrib><creatorcontrib>Sirivichayakul, Sunee</creatorcontrib><creatorcontrib>Matsumoto, Andressa Keiko</creatorcontrib><creatorcontrib>Michelin, Ana Paula</creatorcontrib><creatorcontrib>de Oliveira Semeão, Laura</creatorcontrib><creatorcontrib>de Lima Pedrão, João Victor</creatorcontrib><creatorcontrib>Moreira, Estefania G.</creatorcontrib><creatorcontrib>Barbosa, Decio S.</creatorcontrib><creatorcontrib>Carvalho, Andre F.</creatorcontrib><creatorcontrib>Solmi, Marco</creatorcontrib><creatorcontrib>Kanchanatawan, Buranee</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni 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Database</collection><collection>ProQuest Psychology</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Maes, Michael</au><au>Sirivichayakul, Sunee</au><au>Matsumoto, Andressa Keiko</au><au>Michelin, Ana Paula</au><au>de Oliveira Semeão, Laura</au><au>de Lima Pedrão, João Victor</au><au>Moreira, Estefania G.</au><au>Barbosa, Decio S.</au><au>Carvalho, Andre F.</au><au>Solmi, Marco</au><au>Kanchanatawan, Buranee</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: a Nomothetic Network Psychiatry Approach</atitle><jtitle>Molecular neurobiology</jtitle><stitle>Mol Neurobiol</stitle><date>2020-11-01</date><risdate>2020</risdate><volume>57</volume><issue>11</issue><spage>4578</spage><epage>4597</epage><pages>4578-4597</pages><issn>0893-7648</issn><eissn>1559-1182</eissn><abstract>There is now evidence that schizophrenia and deficit schizophrenia are neuro-immune conditions and that oxidative stress toxicity (OSTOX) may play a pathophysiological role. Aims of the study: to compare OSTOX biomarkers and antioxidant (ANTIOX) defenses in deficit versus non-deficit schizophrenia. We examined lipid hydroperoxides (LOOH), malondialdehyde (MDA), advanced oxidation protein products (AOPP), sulfhydryl (–SH) groups, paraoxonase 1 (PON1) activity and PON1 Q192R genotypes, and total radical-trapping antioxidant parameter (TRAP) as well as immune biomarkers in patients with deficit (
n
= 40) and non-deficit (
n
= 40) schizophrenia and healthy controls (
n
= 40). Deficit schizophrenia is characterized by significantly increased levels of AOPP and lowered –SH, and PON1 activity, while no changes in the OSTOX/ANTIOX biomarkers were found in non-deficit schizophrenia. An increased OSTOX/ANTIOX ratio was significantly associated with deficit versus non-deficit schizophrenia (odds ratio = 3.15,
p
< 0.001). Partial least squares analysis showed that 47.6% of the variance in a latent vector extracted from psychosis, excitation, hostility, mannerism, negative symptoms, psychomotor retardation, formal thought disorders, and neurocognitive test scores was explained by LOOH+AOPP, PON1 genotype + activity, CCL11, tumor necrosis factor (TNF)-α, and IgA responses to neurotoxic tryptophan catabolites (TRYCATs), whereas –SH groups and IgM responses to MDA showed indirect effects mediated by OSTOX and neuro-immune biomarkers. When overall severity of schizophrenia increases, multiple immune and oxidative (especially protein oxidation indicating chlorinative stress) neurotoxicities and impairments in immune-protective resilience become more prominent and shape a distinct nosological entity, namely deficit schizophrenia. The nomothetic network psychiatry approach allows building causal-pathway-phenotype models using machine learning techniques.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s12035-020-02047-5</doi><tpages>20</tpages><orcidid>https://orcid.org/0000-0002-2012-871X</orcidid></addata></record> |
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| subjects | Antioxidants Biomarkers Biomedical and Life Sciences Biomedicine Catabolites Cell Biology Cognition Emotional behavior Genotypes Immunoglobulin A Immunoglobulin M Intellectual disabilities Lipid peroxidation Mental disorders Neurobiology Neurology Neurosciences Neurotoxicity Original Article Oxidative stress Paraoxonase Paraoxonase 1 Phenotypes Psychosis Schizophrenia Tryptophan Tumor necrosis factor-TNF |
| title | Lowered Antioxidant Defenses and Increased Oxidative Toxicity Are Hallmarks of Deficit Schizophrenia: a Nomothetic Network Psychiatry Approach |
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