Abstract
There is some evidence that lowered tryptophan and an activated tryptophan catabolite (TRYCAT) pathway play a role in depression, somatoform disorder, and postpartum blues. The aim of this study is to delineate the associations between the TRYCAT pathway and premenstrual syndrome (PMS) and perinatal depressive and physio-somatic symptoms. We examine the associations between end of term serum IgM and IgA responses to tryptophan and 9 TRYCATs in relation to zinc, C-reactive protein (CRP), and haptoglobin and prenatal physio-somatic (previously known as psychosomatic) symptoms (fatigue, back pain, muscle pain, dyspepsia, obstipation) and prenatal and postnatal depression and anxiety symptoms as measured using the Edinburgh Postnatal Depression Scale (EPDS), Hamilton Depression Rating Scale (HAMD), and Spielberger’s State Anxiety Inventory (STAI). We included pregnant females with (n = 24) and without depression (n = 25) and 24 non-pregnant females. There were no significant associations between the IgA/IgM responses to tryptophan and TRYCATs and prenatal and postnatal depression/anxiety symptoms, except for lowered IgA responses to anthranilic acid in prenatal depression. A large part of the variance in IgA responses to most TRYCATs was explained by PMS and haptoglobin (positively) and CRP (inversely) levels. The IgA responses to TRYCATs were significantly increased in PMS, in particular picolinic, anthranilic, xanthurenic and kynurenic acid, and 3OH-kynurenine. Variance (62.5%) in physio-somatic symptoms at the end of term was explained by PMS, previous depressions, zinc (inversely), CRP and haptoglobin (both positively), and the IgM responses to quinolinic acid (positively), anthranilic acid, and tryptophan (both negatively). The results suggest that mucosa-derived TRYCAT pathway activation is significantly associated with PMS, but not with perinatal depression/anxiety symptoms. Physio-somatic symptoms in pregnancy have an immune-inflammatory pathophysiology. Induction of the TRYCAT pathway appears to be more related to physio-somatic than to depression symptoms.
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Berk M, Williams LJ, Jacka FN, O’Neil A, Pasco JA, Moylan S, Allen NB, Stuart AL, Hayley AC, Byrne ML et al (2013) So depression is an inflammatory disease, but where does the inflammation come from? BMC Med 11:200
Lasoń W, Budziszewska B, Basta-Kaim A, Kubera M, Maes M (2013) New trends in the neurobiology and pharmacology of affective disorders. Pharmacol Rep 65(6):1441–1450
Leonard B, Maes M (2012) Mechanistic explanations how cell-mediated immune activation, inflammation and oxidative and nitrosative stress pathways and their sequels and concomitants play a role in the pathophysiology of unipolar depression. Neurosci Biobehav Rev 36(2):764–785
Maes M, Anderson G, Kubera M, Berk M (2014) Targeting classical IL-6 signalling or IL-6 trans-signalling in depression? Expert Opin Ther Targets 18(5):495–512
Maes M, Kubera M, Leunis JC (2008) The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuroendocrinol Lett 29:117–124
Maes M, Kubera M, Leunis JC, Berk M (2012) Increased IgA and IgM responses against gut commensals in chronic depression: further evidence for increased bacterial translocation or leaky gut. J Affect Disord 141:55–62
Maes M, Scharpé S, Meltzer HY, Okayli G, Bosmans E, D’Hondt P, Vanden Bossche BV, Cosyns P (1994) Increased neopterin and interferon-gamma secretion and lower availability of L-tryptophan in major depression: further evidence for an immune response. Psychiatry Res 54(2):143–160
Maes M, Verkerk R, Vandoolaeghe E, Van Hunsel F, Neels H, Wauters A, Demedts P, Scharpé S (1997) Serotonin-immune interactions in major depression: lower serum tryptophan as a marker of an immune-inflammatory response. Eur Arch Psychiatry Clin Neurosci 247(3):154–161
Moylan S, Berk M, Dean OM, Samuni Y, Williams LJ, O’Neil A, Hayley AC, Pasco JA, Anderson G, Jacka FN et al (2014) Oxidative & nitrosative stress in depression: why so much stress? Neurosci Biobehav Rev 45:46–62
Noto C, Rizzo LB, Mansur RB, McIntyre RS, Maes M, Brietzke E (2014) Targeting the inflammatory pathway as a therapeutic tool for major depression. Neuroimmunomodulation 21(2-3):131–139
Anderson G, Kubera M, Duda W, Lasoń W, Berk M, Maes M (2013) Increased IL-6 trans-signaling in depression: focus on the tryptophan catabolite pathway, melatonin and neuroprogression. Pharmacol Rep 65(6):1647–1654
Dowlati Y, Herrmann N, Swardfager W, Liu H, Sham L, Reim EK et al (2010) A meta-analysis of cytokines in major depression. Biol Psychiatry 67:446–457
Howren MB, Lamkin DM, Suls J (2009) Associations of depression with C-reactive protein, IL-1, and IL-6: a meta-analysis. Psychosom Med 71:171–186
Maes M, Scharpe S, Bosmans E, Vandewoude M, Suy E, Uyttenbroeck W, Cooreman W, Vandervorst C, Raus J (1992) Disturbances in acute phase plasma proteins during melancholia: additional evidence for the presence of an inflammatory process during that illness. Prog Neuropsychopharmacol Biol Psychiatry 16(4):501–515
Haapakoski R, Mathieu J, Ebmeier KP, Alenius H, Kivimäki M (2015) Cumulative meta-analysis of interleukins 6 and 1β, tumour necrosis factor α and C-reactive protein in patients with major depressive disorder. Brain Behav Immun 49:206–215
Anderson G, Berk M, Dean O, Moylan S, Maes M (2014) Role of immune-inflammatory and oxidative and nitrosative stress pathways in the etiology of depression: therapeutic implications. CNS Drugs 28(1):1–10
Maes M, Fisar Z, Medina M, Scapagnini G, Nowak G, Berk M (2012) New drug targets in depression: inflammatory, cell-mediated immune, oxidative and nitrosative stress, mitochondrial, antioxidant, and neuroprogressive pathways. And new drug candidates—Nrf2 activators and GSK-3 inhibitors. Inflammopharmacology 20:127–150
Maes M, Galecki P, Chang YS, Berk M (2011) A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness. Prog Neuropsychopharmacol Biol Psychiatry 35(3):676–692
Jiménez-Fernández S, Gurpegui M, Díaz-Atienza F, Pérez-Costillas L, Gerstenberg M, Correll CU (2015) Oxidative stress and antioxidant parameters in patients with major depressive disorder compared to healthy controls before and after antidepressant treatment: results from a meta-analysis. J Clin Psychiatry 76(12):1658–1667
Sluzewska A, Rybakowski J, Bosmans E, Sobieska M, Berghmans R, Maes M, Wiktorowicz K (1996) Indicators of immune activation in major depression. Psychiatry Res 64(3):161–167
Maes M, Rief W (2012) Diagnostic classifications in depression and somatization should include biomarkers, such as disorders in the tryptophan catabolite (TRYCAT) pathway. Psychiatry Res 196(2-3):243–249
Iseme RA, McEvoy M, Kelly B, Agnew L, Attia J, Walker FR (2014) Autoantibodies and depression: evidence for a causal link? Neurosci Biobehav Rev 40:62–79
Anderson G, Maes M (2015) The gut-brain axis: the role of melatonin in linking psychiatric, inflammatory and neurodegenerative conditions. Adv Integr Med 2(1):31–37
Maes M, Kubera M, Leunis JC, Berk M, Geffard M, Bosmans E (2013) In depression, bacterial translocation may drive inflammatory responses, oxidative and nitrosative stress (O&NS), and autoimmune responses directed against O&NS-damaged neoepitopes. Acta Psychiatr Scand 127(5):344–354
Subero MM, Anderson G, Kanchanatawan B, Berk M, Maes M (2015) Comorbidity between depression and inflammatory bowel disease explained by immune-inflammatory, oxidative and nitrosative stress, tryptophan catabolite and gut-brain pathways. CNS Spectrums 26:1–15
Maes M, Stevens WJ, Declerck LS, Bridts CH, Peeters D, Schotte C, Cosyns P (1993) Significantly increased expression of T-cell activation markers (interleukin-2 and HLA-DR) in depression: further evidence for an inflammatory process during that illness. Prog Neuropsychopharmacol Biol Psychiatry 17(2):241–255
Hood SD, Bell CJ, Nutt DJ (2005) Acute tryptophan depletion. Part I: rationale and methodology. Aust N Z J Psychiatry 39(7):558–564
Toker L, Amar S, Bersudsky Y, Benjamin J, Klein E (2010) The biology of tryptophan depletion and mood disorders. Isr J Psychiatry Relat Sci 47(1):46–55
Maes M, Leonard BE, Myint AM, Kubera M, Verkerk R (2011) The new ‘5-HT’ hypothesis of depression: cell-mediated immune activation induces indoleamine 2,3-dioxygenase, which leads to lower plasma tryptophan and an increased synthesis of detrimental tryptophan catabolites (TRYCATs), both of which contribute to the onset of depression. Prog Neuropsychopharmacol Biol Psychiatry 35(3):702–721
Anderson G, Maes M (2014) Oxidative/nitrosative stress and immuno-inflammatory pathways in depression: treatment implications. Curr Pharm Des 20(23):3812–3847
Anderson G, Maes M, Berk M (2012) Inflammation-related disorders in the tryptophan catabolite pathway in depression and somatization. Adv Protein Chem Struct Biol 88:27–48
Morris G, Carvalho A, Anderson G, Galecki P, Maes M (2015) The many neuroprogressive actions of tryptophan catabolites (TRYCATs) that may be associated with the pathophysiology of neuro-immune disorders. Curr Pharm Des (Epub ahead of print)
Bonaccorso S, Marino V, Puzella A, Pasquini M, Biondi M, Artini M, Almerighi C, Verkerk R, Meltzer H, Maes M (2002) Increased depressive ratings in patients with hepatitis C receiving interferon-alpha-based immunotherapy are related to interferon-alpha-induced changes in the serotonergic system. J Clin Psychopharmacol 22(1):86–90
Maes M, De Ruyter M, Hobin P, Suy E (1987) Relationship between the dexamethasone suppression test and the L-tryptophan/competing amino acids ratio in depression. Psychiatry Res 21(4):323–335
Myint AM, Kim YK, Verkerk R, Scharpé S, Steinbusch H, Leonard B (2007) Kynurenine pathway in major depression: evidence of impaired neuroprotection. J Affect Disord 98(1-2):143–151
Gabbay V, Liebes L, Katz Y, Liu S, Mendoza S, Babb JS, Klein RG, Gonen O (2010) The kynurenine pathway in adolescent depression: preliminary findings from a proton MR spectroscopy study. Prog Neuropsychopharmacol Biol Psychiatry 34(1):37–44
Anderson G, Berk M, Maes M (2014) Biological phenotypes underpin the physio-somatic symptoms of somatization, depression, and chronic fatigue syndrome. Acta Psychiatr Scand 129(2):83–97
Anderson G, Maes M, Berk M (2012) Biological underpinnings of the commonalities in depression, somatization, and chronic fatigue syndrome. Med Hypotheses 78(6):752–756
Maes M, Galecki P, Verkerk R, Rief W (2011) Somatization, but not depression, is characterized by disorders in the tryptophan catabolite (TRYCAT) pathway, indicating increased indoleamine 2,3-dioxygenase and lowered kynurenine aminotransferase activity. Neuro Endocrinol Lett 32(3):264–273
Maes M, Ringel K, Kubera M, Anderson G, Morris G, Galecki P, Geffard M (2013) In myalgic encephalomyelitis/chronic fatigue syndrome, increased autoimmune activity against 5-HT is associated with immuno-inflammatory pathways and bacterial translocation. J Affect Disord 150(2):223–230
Maes M, Verkerk R, Bonaccorso S, Ombelet W, Bosmans E, Scharpé S (2002) Depressive and anxiety symptoms in the early puerperium are related to increased degradation of tryptophan into kynurenine, a phenomenon which is related to immune activation. Life Sci 71(16):1387–1348
Veen C, Myint AM, Burgerhout KM, Schwarz MJ, Schütze G, Kushner SA, Hoogendijk WJ, Drexhage HA, Bergink V (2016) Tryptophan pathway alterations in the postpartum period and in acute postpartum psychosis and depression. J Affect Disord 189:298–305
Bell CJ, Hood SD, Nutt DJ (2005) Acute tryptophan depletion. Part II: clinical effects and implications. Aust N Z J Psychiatry 39(7):565–574
Korzekwa MI, Steiner M (1997) Premenstrual syndromes. Clin Obstet Gynecol 40(3):564–576
Kouri EM, Halbreich U (1997) State and trait serotonergic abnormalities in women with dysphoric premenstrual syndromes. Psychopharmacol Bull 33(4):767–770
Taylor DL, Matthew RJ, Ho BT, Weinman ML (1984) Serotonin levels and platelet uptake during premenstrual tension. Neuropsychobiology 12:16–18
Menkes DB, Coates DC, Fawcett JP (1994) Acute tryptophan depletion aggravates premenstrual syndrome. J Affect Disord 32:37–44
Rapkin AJ, Akopians AL (2012) Pathophysiology of premenstrual syndrome and premenstrual dysphoric disorder. Menopause Int 18(2):52–59
Lolas-Talhami J, Lafaja-Mazuecos J, Ferrández-Sempere D (2015) Is premenstrual syndrome a uterine inflammatory disease? Retrospective evaluation of an etiologic approach. Open J Obstet Gynecol 5:305–312
Bertone-Johnson ER, Ronnenberg AG, Houghton SC, Nobles C, Zagarins SE, Takashima-Uebelhoer BB, Faraj JL, Whitcomb BW (2014) Association of inflammation markers with menstrual symptom severity and premenstrual syndrome in young women. Hum Reprod 29(9):1987–1994
Graziottin A, Zanello PP (2015) Menstruation, inflammation and comorbidities: implications for woman health. Minerva Ginecol 67(1):21–34
Hantsoo L, Epperson CN (2015) Premenstrual dysphoric disorder: epidemiology and treatment. Curr Psychiatry Rep 17(11):87
Puder JJ, Blum CA, Mueller B, De Geyter C, Dye L, Keller U (2006) Menstrual cycle symptoms are associated with changes in low-grade inflammation. Eur J Clin Investig 36:58–64
O’Brien SM, Fitzgerald P, Scully P, Landers A, Scott LV, Dinan TG (2007) Impact of gender and menstrual cycle phase on plasma cytokine concentrations. Neuroimmunomodulation 14:84–90
Northoff H, Symons S, Zieker D, Schaible EV, Schäfer K, Thoma S (2008) Gender- and menstrual phase dependent regulation of inflammatory gene expression in response to aerobic exercise. Exerc Immunol Rev 14:86–103
Gaskins AJ, Wilchesky M, Mumford SL, Whitcomb BW, Browne RW, Wactawski-Wende J, Perkins NJ, Schisterman EF (2012) Endogenous reproductive hormones and C-reactive protein across the menstrual cycle: the BioCycle Study. Am J Epidemiol 175(5):423–431
Wander K, Brindle E, O’Connor KA (2008) C-reactive protein across the menstrual cycle. Am J Phys Anthropol 136(2):138–146
Jane ZY, Chang CC, Lin HK, Liu YC, Chen WL (2011) The association between the exacerbation of irritable bowel syndrome and menstrual symptoms in young Taiwanese women. Gastroenterol Nurs 34:277–286
Kane SV, Sable K, Hanauer SB (1998) The menstrual cycle and its effect on inflammatory bowel disease and irritable bowel syndrome: a prevalence study. Am J Gastroenterol 93:1867–1872
Shourie V, Dwarakanath CD, Prashanth GV, Alampalli RV, Padmanabhan S, Bali S (2012) The effect of menstrual cycle on periodontal health—a clinical and microbiological study. Oral Health Prev Dent 10:185–192
Onodera T, Jang MH, Guo Z, Yamasaki M, Hirata T, Bai Z, Tsuji NM, Nagakubo D, Yoshie O, Sakaguchi S et al (2009) Constitutive expression of IDO by dendritic cells of mesenteric lymph nodes: functional involvement of the CTLA-4/B7 and CCL22/CCR4 interactions. J Immunol 183(9):5608–5614
Cherayil BJ (2009) Indoleamine 2,3-dioxygenase in intestinal immunity and inflammation. Inflamm Bowel Dis 15(9):1391–1396
Anderson G, Maes M (2013) Postpartum depression: psychoneuroimmunological underpinnings and treatment. Neuropsychiatr Dis Treat 9:277–287
Pitanupong J, Liabsuetrakul T, Vittayanont A (2007) Validation of the Thai Edinburgh Postnatal Depression Scale for screening postpartum depression. Psychiatry Res 149(1-3):253–259
Vacharaporn K, Pitanupong J, Samangsri N (2003) Development of The Edinburgh Postnatal Depression Scale Thai Version. J Ment Health Thai 11(3):164–169
Roomruangwong C, Kanchanatawan B, Sirivichayakul S, Mahieu B, Nowak G, Maes M (2016) Lower serum zinc and higher CRP strongly predict prenatal depression and physio-somatic symptoms, which all together predict postnatal depressive symptoms. Mol Neurobiol, Epub ahead of print
Hamilton M (2000) Hamilton Rating Scale for Depression (Ham-D). In: Handbook of psychiatric measures. APA, Washington DC, pp 526–528
Spielberger CD, Vagg PR (1984) Psychometric properties of the STAI: a reply to Ramanaiah, Franzen, and Schill. J Pers Assess 48(1):95–97
Junqueira LC, Carneiro J (2003) Basic Histology: Lange Medical Books McGraw-Hill, New York
Fagarasan S, Honjo T (2003) Intestinal IgA synthesis: regulation of front-line body defenses. Nat Rev Immunol 3(1):63–72
Li DD, Liu XY, Guo CH, Yue L, Yang ZQ, Cao H, Guo B, Yue ZP (2015) Differential expression and regulation of Ido2 in the mouse uterus during peri-implantation period. In Vitro Cell Dev Biol Anim 51(3):264–272
King NJ, Thomas SR (2007) Molecules in focus: indoleamine 2,3-dioxygenase. Int J Biochem Cell Biol 39(12):2167–2172
Mei J, Li MQ, Ding D, Li DJ, Jin LP, Hu WG, Zhu XY (2013) Indoleamine 2,3-dioxygenase-1 (IDO1) enhances survival and invasiveness of endometrial stromal cells via the activation of JNK signaling pathway. Int J Clin Exp Pathol 6(3):431–444
Mei J, Xie XX, Li MQ, Wei CY, Jin LP, Li DJ, Zhu XY (2014) Indoleamine 2,3-dioxygenase-1 (IDO1) in human endometrial stromal cells induces macrophage tolerance through interleukin-33 in the progression of endometriosis. Int J Clin Exp Pathol 7(6):2743–2757
Dürr S, Kindler V (2013) Implication of indolamine 2,3 dioxygenase in the tolerance toward fetuses, tumors, and allografts. J Leukoc Biol 93(5):681–687
Soliman H, Mediavilla-Varela M, Antonia S (2010) Indoleamine 2,3-dioxygenase: is it an immune suppressor? Cancer J 16(4):354–359
MacKenzie G, Maguire J (2014) The role of ovarian hormone-derived neurosteroids on the regulation of GABAA receptors in affective disorders. Psychopharmacology (Berl) 231(17):3333–3342
Studd J (2014) Hormone therapy for reproductive depression in women. Post Reprod Health 20(4):132–137
Studd J, Nappi RE (2012) Reproductive depression. Gynecol Endocrinol 28(Suppl 1):42–45
Turkcapar AF, Kadıoğlu N, Aslan E, Tunc S, Zayıfoğlu M, Mollamahmutoğlu L (2015) Sociodemographic and clinical features of postpartum depression among Turkish women: a prospective study. BMC Pregnancy Childbirth 3(15):108
Watanabe K, Shirakawa T (2015) Characteristics of perceived stress and salivary levels of secretory immunoglobulin A and cortisol in Japanese women with premenstrual syndrome. Nurs Midwifery Stud 4(2):e24795
Kita T, Morrison PF, Heyes MP, Markey SP (2002) Effects of systemic and central nervous system localized inflammation on the contributions of metabolic precursors to the L-kynurenine and quinolinic acid pools in brain. J Neurochem 82(2):258–268
Gavin NI, Gaynes BN, Lohr KN, Meltzer-Brody S, Gartlehner G, Swinson T (2005) Perinatal depression: a systematic review of prevalence and incidence. Obstet Gynecol 106:1071–1083
Stuart-Parrigon K, Stuart S (2014) Perinatal depression: an update and overview. Curr Psychiatry Rep 16(9):468
Rios-Avila L, Nijhout HF, Reed MC, Sitren HS, Gregory JF (2013) A mathematical model of tryptophan metabolism via the kynurenine pathway provides insights into the effects of vitamin B-6 deficiency, tryptophan loading, and induction of tryptophan 2,3-dioxygenase on tryptophan metabolite. J Nutr 143(9):1509–1519
Hoes MJ (1979) The clinical significance of an elevated excretion of xanthurenic acid in psychiatric patients. Acta Psychiatr Belg 79(6):638–646
Darlington LG, Forrest CM, Mackay GM, Smith RA, Smith AJ, Stoy N, Stone TW (2010) On the Biological Importance of the 3-hydroxyanthranilic acid: anthranilic acid ratio. Int J Tryptophan Res 3:51–59
Aqbal D, Abdallah A, Bolloso E, Angerio A: The role of c- reactive protein in inflammatory bowel disease. GUJHS 2007, 4(1). https://blogs.commons.georgetown.edu/journal-of-health-sciences/issue-2/previous-volumes/vol-4-no-1-march-2007/
Harrison M (2015) Erythrocyte sedimentation rate and C-reactive protein. Aust Prescr 38(3):93–94
Zouki C, Beauchamp M, Baron C, Filep JG (1997) Prevention of In vitro neutrophil adhesion to endothelial cells through shedding of L-selectin by C-reactive protein and peptides derived from C-reactive protein. J Clin Invest 100(3):522–529
Gabay C, Kushner I (1999) Acute-phase proteins and other systemic responses to inflammation. N Engl J Med 340(6):448–454
Vermeire S, Van Assche G, Rutgeerts P (2004) C-reactive protein as a marker for inflammatory bowel disease. Inflamm Bowel Dis 10(5):661–665
Badawy AA (2015) Tryptophan metabolism, disposition and utilization in pregnancy. Biosci Rep 35(5):e00261
Shibata K, Fukuwatari T, Murakami M, Sasaki R (2003) Increase in conversion of tryptophan to niacin in pregnant rats. Adv Exp Med Biol 527:435–441
Ban Y, Chang Y, Dong B, Kong B, Qu X (2013) Indoleamine 2,3-dioxygenase levels at the normal and recurrent spontaneous abortion fetal-maternal interface. J Int Med Res 41(4):1135–1149
Maes M, Ombelet W, De Jongh R, Kennis G, Bosman E (2001) The inflammatory response following delivery is amplified in women who previously suffered from major depression, suggesting that major depression is accompanied by a sensitization of the inflammatory response system. J Affect Disord 63:85–92
Alberts B, Johnson A, Lewis J, Walter P, Raff M, Roberts K: Molecular biology of the cell In., 4th edn: Routledge; 2002.
The American Heritage Dictionary (2004) The American Heritage Dictionary of the English Language: Immunoglobulin M, 4th edn: Houghton Mifflin Company, Boston
Maes M (2009) “Functional” or “psychosomatic” symptoms, e.g. a flu-like malaise, aches and pain and fatigue, are major features of major and in particular of melancholic depression. Neuro Endocrinol Lett 30(5):564–573
Groer MW, Morgan K (2007) Immune, health and endocrine characteristics of depressed postpartum mothers. Psychoneuroendocrinology 32(2):133–139
Wichers MC, Koek GH, Robaeys G, Praamstra AJ, Maes M (2005) Early increase in vegetative symptoms predicts IFN-alpha-induced cognitive-depressive changes. Psychol Med 35(3):433–441
O’Connor E, Rossom RC, Henninger M, Groom HC, Burda BU (2016) Primary care screening for and treatment of depression in pregnant and postpartum women: evidence report and systematic review for the US Preventive Services Task Force. JAMA 315(4):388–406
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This research has been supported by the Ratchadaphiseksomphot Endowment Fund 2013 of Chulalongkorn University (CU-56-457-HR)
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Roomruangwong, C., Kanchanatawan, B., Sirivichayakul, S. et al. IgA/IgM responses to tryptophan and tryptophan catabolites (TRYCATs) are differently associated with prenatal depression, physio-somatic symptoms at the end of term and premenstrual syndrome. Mol Neurobiol 54, 3038–3049 (2017). https://doi.org/10.1007/s12035-016-9877-3
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DOI: https://doi.org/10.1007/s12035-016-9877-3