Michael Maes, Ketsupar Jirakran, Laura de Oliveira Semeão, Ana Paula Michelin, Andressa K Matsumoto, Francis F Brinholi, Decio S Barbosa, Chavit Tivirachaisakul, Abbas F Almulla, Drozdstoj Stoyanov, Yingqian Zhang
{"title":"门诊患者神经免疫代谢氧化（NIMETOX）重度抑郁症的关键因素：对氧磷酶1活性、胆固醇转运逆转、动脉粥样硬化性增加、蛋白质氧化和不同表达的细胞因子网络。","authors":"Michael Maes, Ketsupar Jirakran, Laura de Oliveira Semeão, Ana Paula Michelin, Andressa K Matsumoto, Francis F Brinholi, Decio S Barbosa, Chavit Tivirachaisakul, Abbas F Almulla, Drozdstoj Stoyanov, Yingqian Zhang","doi":"","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>Major depressive disorder (MDD) is associated with neuro-immune - metabolic - oxidative (NIMETOX) pathways.</p><p><strong>Aims: </strong>To examine the connections among NIMETOX pathways in outpatient MDD (OMDD) with and without metabolic syndrome (MetS); and to determine the prevalence of NIMETOX aberrations in a cohort of OMDD patients.</p><p><strong>Methods: </strong>We included 67 healthy controls and 66 OMDD patients and we assessed various NIMETOX pathways.</p><p><strong>Results: </strong>We successfully identified a subgroup of individuals with aberrations in NIMETOX pathways, including diminished lecithin-cholesterol acyltransferase (LCAT), paraoxonase 1 (PON1) activity, and reverse cholesterol transport (RCT) activities, and elevated atherogenicity, differentially expressed immune networks, and advanced oxidation protein products (AOPP). A large part of the variance (around 44%) in atherogenicity indices was associated with AOPP, fasting blood glucose (FBG), PON1 activity, and immune activation. LCAT activity was positively correlated with PON1 activity and negatively with FBG, AOPP and immune activation. RCT was positively related with the PON1 R/R 192 genotype and negatively with FBG and immune activation. A larger part of the variance in the overall severity of OMDD (50.4%), suicidal behaviors (27.7%), and neuroticism (42.1%) was positively associated with adverse childhood experiences and NIMETOX pathways, including AOPP, immune-related neurotoxicity, FBG, insulin, and atherogenicity, and inversely with immune-related neuroprotection.</p><p><strong>Conclusions: </strong>Many OMDD patients (78.8%) show aberrations in NIMETOX pathways. The features of OMDD, including severity of illness, neuroticism, and suicidal behaviors, are caused by intertwined NIMETOX pathways that may exert additional effects depending on whether MetS is present or not.</p>","PeriodicalId":94154,"journal":{"name":"Neuro endocrinology letters","volume":"46 2","pages":"115-125"},"PeriodicalIF":0.6000,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Key factors underpinning neuroimmune-metabolic-oxidative (NIMETOX) major depression in outpatients: paraoxonase 1 activity, reverse cholesterol transport, increased atherogenicity, protein oxidation, and differently expressed cytokine networks.\",\"authors\":\"Michael Maes, Ketsupar Jirakran, Laura de Oliveira Semeão, Ana Paula Michelin, Andressa K Matsumoto, Francis F Brinholi, Decio S Barbosa, Chavit Tivirachaisakul, Abbas F Almulla, Drozdstoj Stoyanov, Yingqian Zhang\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Major depressive disorder (MDD) is associated with neuro-immune - metabolic - oxidative (NIMETOX) pathways.</p><p><strong>Aims: </strong>To examine the connections among NIMETOX pathways in outpatient MDD (OMDD) with and without metabolic syndrome (MetS); and to determine the prevalence of NIMETOX aberrations in a cohort of OMDD patients.</p><p><strong>Methods: </strong>We included 67 healthy controls and 66 OMDD patients and we assessed various NIMETOX pathways.</p><p><strong>Results: </strong>We successfully identified a subgroup of individuals with aberrations in NIMETOX pathways, including diminished lecithin-cholesterol acyltransferase (LCAT), paraoxonase 1 (PON1) activity, and reverse cholesterol transport (RCT) activities, and elevated atherogenicity, differentially expressed immune networks, and advanced oxidation protein products (AOPP). A large part of the variance (around 44%) in atherogenicity indices was associated with AOPP, fasting blood glucose (FBG), PON1 activity, and immune activation. LCAT activity was positively correlated with PON1 activity and negatively with FBG, AOPP and immune activation. RCT was positively related with the PON1 R/R 192 genotype and negatively with FBG and immune activation. A larger part of the variance in the overall severity of OMDD (50.4%), suicidal behaviors (27.7%), and neuroticism (42.1%) was positively associated with adverse childhood experiences and NIMETOX pathways, including AOPP, immune-related neurotoxicity, FBG, insulin, and atherogenicity, and inversely with immune-related neuroprotection.</p><p><strong>Conclusions: </strong>Many OMDD patients (78.8%) show aberrations in NIMETOX pathways. The features of OMDD, including severity of illness, neuroticism, and suicidal behaviors, are caused by intertwined NIMETOX pathways that may exert additional effects depending on whether MetS is present or not.</p>\",\"PeriodicalId\":94154,\"journal\":{\"name\":\"Neuro endocrinology letters\",\"volume\":\"46 2\",\"pages\":\"115-125\"},\"PeriodicalIF\":0.6000,\"publicationDate\":\"2025-09-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuro endocrinology letters\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuro endocrinology letters","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Key factors underpinning neuroimmune-metabolic-oxidative (NIMETOX) major depression in outpatients: paraoxonase 1 activity, reverse cholesterol transport, increased atherogenicity, protein oxidation, and differently expressed cytokine networks.
Background: Major depressive disorder (MDD) is associated with neuro-immune - metabolic - oxidative (NIMETOX) pathways.
Aims: To examine the connections among NIMETOX pathways in outpatient MDD (OMDD) with and without metabolic syndrome (MetS); and to determine the prevalence of NIMETOX aberrations in a cohort of OMDD patients.
Methods: We included 67 healthy controls and 66 OMDD patients and we assessed various NIMETOX pathways.
Results: We successfully identified a subgroup of individuals with aberrations in NIMETOX pathways, including diminished lecithin-cholesterol acyltransferase (LCAT), paraoxonase 1 (PON1) activity, and reverse cholesterol transport (RCT) activities, and elevated atherogenicity, differentially expressed immune networks, and advanced oxidation protein products (AOPP). A large part of the variance (around 44%) in atherogenicity indices was associated with AOPP, fasting blood glucose (FBG), PON1 activity, and immune activation. LCAT activity was positively correlated with PON1 activity and negatively with FBG, AOPP and immune activation. RCT was positively related with the PON1 R/R 192 genotype and negatively with FBG and immune activation. A larger part of the variance in the overall severity of OMDD (50.4%), suicidal behaviors (27.7%), and neuroticism (42.1%) was positively associated with adverse childhood experiences and NIMETOX pathways, including AOPP, immune-related neurotoxicity, FBG, insulin, and atherogenicity, and inversely with immune-related neuroprotection.
Conclusions: Many OMDD patients (78.8%) show aberrations in NIMETOX pathways. The features of OMDD, including severity of illness, neuroticism, and suicidal behaviors, are caused by intertwined NIMETOX pathways that may exert additional effects depending on whether MetS is present or not.
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