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Fatty acids in contextNeurometabolic perspectives on depression vulnerabilityMocking, R.J.T.

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Citation for published version (APA):Mocking, R. J. T. (2017). Fatty acids in context: Neurometabolic perspectives on depression vulnerability.

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Discussion of emotional processing

Summary of our findingsIn sum, we showed that unmedicated depressed and remitted patients with MDD or bipolar disease showed transdiagnostic differences and similarities in emotional processing and related brain activity depending on the symptomatic state of the disease. In the remitted state, only bipolar patients showed impaired emotion regulation, associated with increased dorsolateral prefrontal cortex activity. During the depressed state, patients with bipolar disease performed worse than those with MDD on sad emotion regulation but better on happy emotion regulation, and they demonstrated significantly less rostral anterior cingulate activity while regulating happy compared with sad emotions. These transdiagnostic differences and similarities in emotional processing and related brain activity contribute to disease understanding, and if replicated they may ultimately be used to reduce heterogeneity and thereby improve diagnostic classification of mood disoders patients.

Relation with other literatureEmotional processing remains a concept at the heart of MDD. Functional MRI studies on emotional processing provide increasing evidence for the importance of a network perspective.222,223 The field moved from modern phrenology (assessing sizes and activities of specified brain regions) to a circuits/network/connectomics approach. Meta-analyses corroborate reduced connectivity within frontoparietal control systems, together with an imbalanced connectivity with other networks involved in emotional processing,149,150,224 that may be due to altered glutamatergic metabolism.225,226 However, transdiagnostic meta-analysis question the specificity of these alterations for MDD.227

In the DELTA-neuroimaging study, we showed that daily real-life dynamics in positive and negative affect were related to brain network organization in remitted recurrent MDD, as recently published in Neuropsychopharmacology.228 In brief, remitted recurrent MDD patients, compared to healthy controls, were less stable in symptoms related to negative affect and these dynamics were associated with differences in information processing within and between specific functional brain subnetworks. These results are a first step to gain a better understanding of how emotion fluctuations in real-life are represented in the brain and provide insights in emotional processing vulnerability profiles of MDD.

Several additional investigations are going on to gain further insight in alterations in brain functioning and structure associated with emotional processing biases in MDD. Especially the use of novel analytical approaches will ensure that data will be used efficiently. These new analytical techniques hopefully work around important statistical concerns about false-positive findings in MRI findings.229 These statistical concerns may explain the limited or even absent clinical translation of MRI in psychiatry.230,231 Nevertheless, ultimately MRI may be used to inform clinicians on clinical course, and provide targets to modulate it. Some aspiring ideas have already been put forward. For example, resting state fMRI was able to predict outcome of electroconvulsive therapy in MDD with ~85% sensitivity and specificity.232 Functional MRI responses to emotional faces predicted naturalistic course of MDD with up to 73% accuracy.233 Finally, resting state functional connectivity distinguished

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MDD from BD with ~70% accuracy.234 However, accuracies are usually not high enough for clinical implementation yet, even if they can be replicated. ‘Smarter’ combination and integration of data may result in more clinically usable tools.235,236

Clinical translation of emotional processing theories have also been attempted using neuropsychological test batteries quantitatively measuring biases in emotional processing without relying on expensive MRI techniques.135 For example, in Neuropsychopharmacology we described our use of an emotional processing test battery to test the depressogenic effects of the smoking cessation drug varenicline. A lack of effects of varenicline on this sensitive emotional processing battery in non-smoking participants suggests that any clinical depressogenic effects are caused by successfully stopping smoking itself.237 On the contrary, the same emotional processing battery proved to be able to detect the clinically relevant depressogenic effects of rimonabant.238 Moreover, in the DELTA-Neuroimaging study we currently test whether emotional processing alterations seen in remitted MDD can predict recurrence,239 and efforts to predict antidepressant response from emotional processing are underway.135

ConclusionDisturbances in emotional processing are an essential feature of MDD. These emotional processing alterations seem associated with imbalances in brain network connectivity, mainly between controlling frontoparietal and limbic ventral networks. Neuropsychological emotional processing test batteries are being used to predict clinically relevant outcomes. Transdiagnostic studies suggest limited specificity and inconsistencies remain, which may be improved by statistically robust replication. Nevertheless, initial aspiring findings show that neuroimaging correlates of emotional processing still has great potential to increase disease understanding and thereby reduce heterogeneity and personalize medicine.

Overall conclusion

In this third Part we described our research on two main pathophysiological aspects in MDD: neuroendocrinological stress and emotional processing. Research in both areas showed interesting alterations, but important inconsistencies remain. Initial initiatives to use these pathophysiological aspects to personalize treatment and/or prognosis or as targets for interventions have been made, but are not robust enough yet for clinical implementation.

Interestingly, these two aspects have both been hypothesized to be (patho)physiologically linked with fatty acid metabolism. Nevertheless, most studies investigated these aspects in isolation. Taking these links between pathophysiological aspects into account could provide an important way to improve consistency in findings. In the next Part of this thesis, we will explain the possible links with fatty acid metabolism, and present our data investigating these links.

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REFERENCE LIST

1. Maninger N, Wolkowitz OM, Reus VI, Epel ES, Mellon SH. Neurobiological and neuropsychiatric effects of dehydroepiandrosterone (DHEA) and DHEA sulfate (DHEAS). Front. Neuroendocrinol. 2009;30(1):65-91.

2. Kudielka BM, Hellhammer DH, Wüst S. Why do we respond so differently? Reviewing determinants of human salivary cortisol responses to challenge. Psychoneuroendocrinology.34(1):2-18.

3. Clow A, Hucklebridge F, Stalder T, Evans P, Thorn L. The cortisol awakening response: more than a measure of HPA axis function. Neurosci. Biobehav. Rev. 2010;35(1):97-103.

4. Vreeburg SA, Hoogendijk WJ, van Pelt J, et al. Major depressive disorder and hypothalamic-pituitary-adrenal axis activity: results from a large cohort study. Archives of general psychiatry. 2009;66(6):617-626.

5. Holsboer F. The corticosteroid receptor hypothesis of depression. Neuropsychopharmacology. 2000;23(5):477-501.

6. McEwen BS. Physiology and neurobiology of stress and adaptation: central role of the brain. Physiol. Rev. 2007;87(3):873-904.

7. Gold PW, Loriaux DL, Roy A, et al. Responses to corticotropin-releasing hormone in the hypercortisolism of depression and Cushing’s disease. Pathophysiologic and diagnostic implications. N. Engl. J. Med. 1986;314(21):1329-1335.

8. Knorr U, Vinberg M, Kessing LV, Wetterslev J. Salivary cortisol in depressed patients versus control persons: a systematic review and meta-analysis. Psychoneuroendocrinology. 2010;35(9):1275-1286.

9. Pariante CM, Miller AH. Glucocorticoid receptors in major depression: relevance to pathophysiology and treatment. Biol Psychiatry. 2001;49(5):391-404.

10. Rubin RT, Phillips JJ, Sadow TF, McCracken JT. Adrenal gland volume in major depression. Increase during the depressive episode and decrease with successful treatment. Archives of general psychiatry. 1995;52(3):213-218.

11. Stetler C, Miller GE. Depression and hypothalamic-pituitary-adrenal activation: a quantitative summary of four decades of research. Psychosom. Med. 2011;73(2):114-126.

12. Strickland PL, Deakin JFW, Percival C, Dixon J, Gater RA, Goldberg DP. Bio-social origins of depression in the community - Interactions between social adversity, cortisol and serotonin neurotransmission. Br. J. Psychiatry. 2002;180:168-173.

13. Ahrens T, Deuschle M, Krumm B, van der Pompe G, den Boer JA, Lederbogen F. Pituitary-adrenal and sympathetic nervous system responses to stress in women remitted from recurrent major depression. Psychosom. Med. 2008;70(4):461-467.

14. Carpenter LL, Ross NS, Tyrka AR, Anderson GM, Kelly M, Price LH. Dex/CRH test cortisol response in outpatients with major depression and matched healthy controls. Psychoneuroendocrinology. 2009;34(8):1208-1213.

15. Oquendo MA, Echavarria G, Galfalvy HC, et al. Lower cortisol levels in depressed patients with comorbid post-traumatic stress disorder. Neuropsychopharmacology. 2003;28(3):591-598.

16. Starckmann MN. Psychiatric manifestations of hyperadrenocorticism and hypoadrenocorticism (Cushing’s and Addeson’s diseases). In: Wolkowitz OM, Rothschild AJ, eds. Psychoneuroendocrinology. Washington, DC: Americ Psychiatric Publishing, Inc.; 2003:165-188.

17. Wolkowitz OM, Burke H, Epel ES, Reus VI. Glucocorticoids. Mood, memory, and mechanisms. Ann. N. Y. Acad. Sci. 2009;1179:19-40.

18. Pariante CM. Risk factors for development of depression and psychosis. Glucocorticoid receptors and pituitary implications for treatment with antidepressant and glucocorticoids. Ann. N. Y. Acad. Sci. 2009;1179:144-152.

19. Bhagwagar Z, Cowen PJ. ‘It’s not over when it’s over’: persistent neurobiological abnormalities in recovered depressed patients. Psychol. Med. 2008;38(3):307-313.

20. Greden JF. The burden of recurrent depression: causes, consequences, and future prospects. The Journal of clinical psychiatry. 2001;62 Suppl 22:5-9.

21. Bockting CL, Spinhoven P, Koeter MW, Wouters LF, Schene AH, Depression Evaluation Longitudinal Therapy Assessment Study G. Prediction of recurrence in recurrent depression and the influence of consecutive episodes on vulnerability for depression: a 2-year prospective study. The Journal of clinical psychiatry. 2006;67(5):747-755.

22. Van Den Eede F, Van den Bossche B, Hulstijn W, Sabbe BG, Cosyns P, Claes SJ. Combined dexamethasone/CRF test in remitted outpatients with recurrent major depressive disorder. J. Affect. Disord. 2006;93(1-3):259-263.

127

23. Zobel AW, Nickel T, Sonntag A, Uhr M, Holsboer F, Ising M. Cortisol response in the combined dexamethasone/CRH test as predictor of relapse in patients with remitted depression: a prospective study. J. Psychiatr. Res. 2001;35(2):83-94.

24. Appelhof BC, Huyser J, Verweij M, et al. Glucocorticoids and relapse of major depression (dexamethasone/corticotropin-releasing hormone test in relation to relapse of major depression). Biol Psychiatry. 2006;59(8):696-701.

25. 2Goodyer IM, Herbert J, Tamplin A, Altham PM. Recent life events, cortisol, dehydroepiandrosterone and the onset of major depression in high-risk adolescents. Br. J. Psychiatry. 2000;177:499-504.

26. Bockting CL, Schene AH, Spinhoven P, et al. Preventing relapse/recurrence in recurrent depression with cognitive therapy: a randomized controlled trial. J. Consult. Clin. Psychol. 2005;73(4):647-657.

27. Hsiao FH, Jow GM, Lai YM, et al. The long-term effects of psychotherapy added to pharmacotherapy on morning to evening diurnal cortisol patterns in outpatients with major depression. Psychother. Psychosom. 2011;80(3):166-172.

28. Heim C, Newport DJ, Bonsall R, Miller AH, Nemeroff CB. Altered pituitary-adrenal axis responses to provocative challenge tests in adult survivors of childhood abuse. Am. J. Psychiatry. 2001;158(4):575-581.

29. Kendler KS, Thornton LM, Gardner CO. Stressful life events and previous episodes in the etiology of major depression in women: an evaluation of the “kindling” hypothesis. Am. J. Psychiatry. 2000;157(8):1243-1251.

30. Matthews SG. Early programming of the hypothalamo-pituitary-adrenal axis. Trends Endocrinol. Metab. 2002;13(9):373-380.

31. Hasler G, Drevets WC, Manji HK, Charney DS. Discovering endophenotypes for major depression. Neuropsychopharmacology. 2004;29(10):1765-1781.

32. Mannie ZN, Harmer CJ, Cowen PJ. Increased waking salivary cortisol levels in young people at familial risk of depression. Am. J. Psychiatry. 2007;164(4):617-621.

33. Holsboer F, Lauer CJ, Schreiber W, Krieg JC. Altered Hypothalamic-Pituitary-Adrenocortical Regulation in Healthy-Subjects at High Familial Risk for Affective-Disorders. Neuroendocrinology. 1995;62(4):340-347.

34. Bartels M, Van den Berg M, Sluyter F, Boomsma DI, de Geus EJ. Heritability of cortisol levels: review and simultaneous analysis of twin studies. Psychoneuroendocrinology. 2003;28(2):121-137.

35. Irving I. Gottesman, Todd D. Gould. The Endophenotype Concept in Psychiatry: Etymology and Strategic Intentions. Am. J. Psychiatry. 2003;160(4):636-645.

36. First MB, Gibbon M, Spitzer RL, Williams JB. User Guide for the Structured Clinical Interview for DSM-IV Axis-1 Disorders. Washington, DC: American Psychiatric Association; 1996.

37. Hamilton M. A rating scale for depression. Journal of neurology, neurosurgery, and psychiatry. 1960;23:56-62.

38. Kraaij V, de Wilde EJ. Negative life events and depressive symptoms in the elderly: a life span perspective. Aging & mental health. 2001;5(1):84-91.

39. Kraaij V, Garnefski N, de Wilde EJ, et al. Negative Life Events and Depressive Symptoms in Late Adolescence: Bonding and Cognitive Coping as Vulnerability Factors? Journal of Youth and Adolescence. 2003;32(3):185-193.

40. Vingerhoets AJJM, van Tilburg MAL. Everyday Problem Checklist (EPCL). Lisse: Swets & Zeitlinger BV.

41. Beck AT, Rush AJ, Shaw BF, Emery G. Cognitive therapy of depression. New York: Guilford; 1979.

42. Hakkaart-van Roijen L, van Straten A, Donker M, Tiemens B. Manual Trimbos/IMTA questionnaire for Costs associated with Psychiatric Illness (TIC-P). Erasmus University Rotterdam: Institute for Medical Technology Assessment; 2002.

43. Bockting CL, ten Doesschate MC, Spijker J, et al. Continuation and maintenance use of antidepressants in recurrent depression. Psychother. Psychosom. 2008;77(1):17-26.

44. Kirschbaum C, Hellhammer DH. Salivary cortisol in psychoneuroendocrine research: recent developments and applications. Psychoneuroendocrinology. 1994;19(4):313-333.

45. AMELIA II: A Program for Missing Data 2010.46. Donders AR, van der Heijden GJ, Stijnen T,

Moons KG. Review: a gentle introduction to imputation of missing values. J. Clin. Epidemiol. 2006;59(10):1087-1091.

47. Rosenbaum PR, Rubin DB. The Central Role of the Propensity Score in Observational Studies for Causal Effects. Biometrika. 1983;70(1):41-55.

48. Vreeburg SA, Kruijtzer BP, van Pelt J, et al. Associations between sociodemographic, sampling and health factors and various salivary cortisol indicators in a large sample without psychopathology. Psychoneuroendocrinology. 2009;34(8):1109-1120.

49. Gueorguieva R, Krystal JH. Move over ANOVA: progress in analyzing repeated-measures data and its reflection in papers published in the Archives of General Psychiatry. Archives of general psychiatry. 2004;61(3):310-317.

III

128

50. MI-mul.sps [Computer code] [computer program]. 2006.

51. Bhagwagar Z, Hafizi S, Cowen PJ. Increase in concentration of waking salivary cortisol in recovered patients with depression. Am. J. Psychiatry. 2003;160(10):1890-1891.

52. Modell S, Lauer CJ, Schreiber W, Huber J, Krieg JC, Holsboer F. Hormonal response pattern in the combined DEX-CRH test is stable over time in subjects at high familial risk for affective disorders. Neuropsychopharmacology. 1998;18(4):253-262.

53. Schule C, Baghai TC, Eser D, Schwarz M, Bondy B, Rupprecht R. Effects of mirtazapine on dehydroepiandrosterone-sulfate and cortisol plasma concentrations in depressed patients. Journal of psychiatric research. 2009;43(5):538-545.

54. Manthey L, Leeds C, Giltay EJ, et al. Antidepressant use and salivary cortisol in depressive and anxiety disorders. Eur. Neuropsychopharmacol. 2011;21(9):691-699.

55. Deuschle M, Hamann B, Meichel C, et al. Antidepressive treatment with amitriptyline and paroxetine: effects on saliva cortisol concentrations. J. Clin. Psychopharmacol. 2003;23(2):201-205.

56. Heim C, Ehlert U, Hellhammer DH. The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders. Psychoneuroendocrinology. 2000;25(1):1-35.

57. Fries E, Hesse J, Hellhammer J, Hellhammer DH. A new view on hypocortisolism. Psychoneuroendocrinology. 2005;30(10):1010-1016.

58. Nesse RM. Is depression an adaptation? Arch. Gen. Psychiatry. 2000;57(1):14-20.

59. Putman P, Roelofs K. Effects of single cortisol administrations on human affect reviewed: Coping with stress through adaptive regulation of automatic cognitive processing. Psychoneuroendocrinology. 2011;36(4):439-448.

60. Bouhuys AL, Bos EH, Geerts E, van Os TW, Ormel J. The association between levels of cortisol secretion and fear perception in patients with remitted depression predicts recurrence. J. Nerv. Ment. Dis. 2006;194(7):478-484.

61. Aubry JM, Gervasoni N, Osiek C, et al. The DEX/CRH neuroendocrine test and the prediction of depressive relapse in remitted depressed outpatients. Journal of psychiatric research. 2007;41(3-4):290-294.

62. Hatzinger M, Hemmeter UM, Baumann K, Brand S, Holsboer-Trachsler E. The combined DEX-CRH test in treatment course and long-term outcome of major depression. Journal of psychiatric research. 2002;36(5):287-297.

63. Bockting CL, Spinhoven P, Wouters LF, Koeter MW, Schene AH, Group DS. Long-term effects of preventive cognitive therapy in recurrent depression: a 5.5-year follow-up study. The Journal of clinical psychiatry. 2009;70(12):1621-1628.

64. Yang TT, Hsiao FH, Wang KC, et al. The effect of psychotherapy added to pharmacotherapy on cortisol responses in outpatients with major depressive disorder. J. Nerv. Ment. Dis. 2009;197(6):401-406.

65. Bockting CL, Spinhoven P, Koeter MW, et al. Differential predictors of response to preventive cognitive therapy in recurrent depression: a 2-year prospective study. Psychother. Psychosom. 2006;75(4):229-236.

66. Galobardes B, Morabia A, Bernstein MS. The Differential Effect of Education and Occupation on Body Mass and Overweight in a Sample of Working People of the General Population. Ann. Epidemiol. 2000;10(8):532-537.

67. Wardenaar KJ, van Veen T, Giltay EJ, de Beurs E, Penninx BW, Zitman FG. Development and validation of a 30-item short adaptation of the Mood and Anxiety Symptoms Questionnaire (MASQ). Psychiatry Res. 2010;179(1):101-106.

68. Assies J, Mocking RJ, Lok A, Ruhe HG, Pouwer F, Schene AH. Effects of oxidative stress on fatty acid- and one-carbon-metabolism in psychiatric and cardiovascular disease comorbidity. Acta psychiatrica Scandinavica. 2014;130(3):163-180.

69. Lok A, Mocking RJ, Ruhe HG, et al. Longitudinal hypothalamic-pituitary-adrenal axis trait and state effects in recurrent depression. Psychoneuroendocrinology. 2012;37(7):892-902.

70. Genud R, Merenlender A, Gispan-Herman I, Maayan R, Weizman A, Yadid G. DHEA lessens depressive-like behavior via GABA-ergic modulation of the mesolimbic system. Neuropsychopharmacology. 2009;34(3):577-584.

71. Sakr HF, Khalil KI, Hussein AM, Zaki MS, Eid RA, Alkhateeb M. Effect of dehydroepiandrosterone (DHEA) on memory and brain derived neurotrophic factor (BDNF) in a rat model of vascular dementia. J. Physiol. Pharmacol. 2014;65(1):41-53.

72. Chen FR, Raine A, Granger DA. Tactics for modeling multiple salivary analyte data in relation to behavior problems: Additive, ratio, and interaction effects. Psychoneuroendocrinology. 2015;51C(0):188-200.

73. Lennartsson AK, Theorell T, Kushnir MM, Bergquist J, Jonsdottir IH. Perceived stress at work is associated with attenuated DHEA-S response during acute psychosocial stress. Psychoneuroendocrinology. 2013;38(9):1650-1657.

74. Young AH, Gallagher P, Porter RJ. Elevation of the cortisol-dehydroepiandrosterone ratio in drug-free depressed patients. Am. J. Psychiatry. 2002;159(7):1237-1239.

129

75. Assies J, Visser I, Nicolson NA, et al. Elevated salivary dehydroepiandrosterone-sulfate but normal cortisol levels in medicated depressed patients: preliminary findings. Psychiatry Res. 2004;128(2):117-122.

76. Juster RP, McEwen BS, Lupien SJ. Allostatic load biomarkers of chronic stress and impact on health and cognition. Neurosci. Biobehav. Rev. 2010;35(1):2-16.

77. Bockting CL, Lok A, Visser I, et al. Lower cortisol levels predict recurrence in remitted patients with recurrent depression: a 5.5 year prospective study. Psychiatry Res. 2012;200(2-3):281-287.

78. Whetzel CA, Klein LC. Measuring DHEA-S in saliva: time of day differences and positive correlations between two different types of collection methods. BMC Res. Notes. 2010;3:204.

79. Bland JM, Altman DG. Measurement error proportional to the mean. BMJ. 1996;313(7049):106.

80. Heuser I, Deuschle M, Luppa P, Schweiger U, Standhardt H, Weber B. Increased diurnal plasma concentrations of dehydroepiandrosterone in depressed patients. J. Clin. Endocrinol. Metab. 1998;83(9):3130-3133.

81. Girdler SS, Lindgren M, Porcu P, Rubinow DR, Johnson JL, Morrow AL. A history of depression in women is associated with an altered GABAergic neuroactive steroid profile. Psychoneuroendocrinology. 2012;37(4):543-553.

82. Ritsner M, Gibel A, Maayan R, et al. State and trait related predictors of serum cortisol to DHEA(S) molar ratios and hormone concentrations in schizophrenia patients. Eur. Neuropsychopharmacol. 2007;17(4):257-264.

83. Michael A, Jenaway A, Paykel ES, Herbert J. Altered salivary dehydroepiandrosterone levels in major depression in adults. Biol Psychiatry. 2000;48(10):989-995.

84. Fabian TJ, Dew MA, Pollock BG, et al. Endogenous concentrations of DHEA and DHEA-S decrease with remission of depression in older adults. Biol Psychiatry. 2001;50(10):767-774.

85. Hsiao CC. Difference in pre- and post-treatment plasma DHEA levels were significantly and positively correlated with difference in pre- and post-treatment Hamilton depression scores following successful therapy for major depression. Psychoneuroendocrinology. 2006;31(7):839-846.

86. Morita T, Senzaki K, Ishihara R, et al. Plasma dehydroepiandrosterone sulfate levels in patients with major depressive disorder correlate with remission during treatment with antidepressants. Human psychopharmacology. 2014;29(3):280-286.

87. Paslakis G, Luppa P, Gilles M, et al. Venlafaxine and mirtazapine treatment lowers serum concentrations of dehydroepiandrosterone-sulfate in depressed patients remitting during the course of treatment. Journal of psychiatric research. 2010;44(8):556-560.

88. Goodyer IM, Herbert J, Tamplin A. Psychoendocrine antecedents of persistent first-episode major depression in adolescents: a community-based longitudinal enquiry. Psychol. Med. 2003;33(4):601-610.

89. Kurita H, Maeshima H, Kida S, et al. Serum dehydroepiandrosterone (DHEA) and DHEA-sulfate (S) levels in medicated patients with major depressive disorder compared with controls. J. Affect. Disord. 2013;146(2):205-212.

90. Markopoulou K, Papadopoulos A, Juruena MF, Poon L, Pariante CM, Cleare AJ. The ratio of cortisol/DHEA in treatment resistant depression. Psychoneuroendocrinology. 2009;34(1):19-26.

91. Ruhe HG, Khoenkhoen SJ, Ottenhof KW, Koeter MW, Mocking RJ, Schene AH. Longitudinal effects of the SSRI paroxetine on salivary cortisol in Major Depressive Disorder. Psychoneuroendocrinology. 2015;52:261-271.

92. Pariante CM. The role of multi-drug resistance p-glycoprotein in glucocorticoid function: studies in animals and relevance in humans. Eur. J. Pharmacol. 2008;583(2-3):263-271.

93. Pariante CM, Thomas SA, Lovestone S, Makoff A, Kerwin RW. Do antidepressants regulate how cortisol affects the brain? Psychoneuroendocrinology. 2004;29(4):423-447.

94. Bortfeld M, Rius M, Konig J, Herold-Mende C, Nies AT, Keppler D. Human multidrug resistance protein 8 (MRP8/ABCC11), an apical efflux pump for steroid sulfates, is an axonal protein of the CNS and peripheral nervous system. Neuroscience. 2006;137(4):1247-1257.

95. Zelcer N, Reid G, Wielinga P, et al. Steroid and bile acid conjugates are substrates of human multidrug-resistance protein (MRP) 4 (ATP-binding cassette C4). Biochem. J. 2003;371(Pt 2):361-367.

96. Sripada RK, Marx CE, King AP, et al. DHEA enhances emotion regulation neurocircuits and modulates memory for emotional stimuli. Neuropsychopharmacology. 2013;38(9):1798-1807.

97. Mouthaan J, Sijbrandij M, Luitse JS, Goslings JC, Gersons BP, Olff M. The role of acute cortisol and DHEAS in predicting acute and chronic PTSD symptoms. Psychoneuroendocrinology. 2014;45:179-186.

98. Olff M, de Vries GJ, Guzelcan Y, Assies J, Gersons BP. Changes in cortisol and DHEA plasma levels after psychotherapy for PTSD. Psychoneuroendocrinology. 2007;32(6):619-626.

III

130

99. Lamers F, Vogelzangs N, Merikangas KR, de Jonge P, Beekman AT, Penninx BW. Evidence for a differential role of HPA-axis function, inflammation and metabolic syndrome in melancholic versus atypical depression. Mol Psychiatry. 2013;18(6):692-699.

100. Whetzel CA, Klein LC. A functional assessment of salivary dehydroepiandrosterone sulfate (DHEA-S) in response to acute stresss. [University Park, Pa.]: Pennsylvania State University; 2008: http://etda.libraries.psu.edu/theses/approved/WorldWideIndex/ETD-3002/index.html.

101. Stewart PM. Aging and fountain-of-youth hormones. N. Engl. J. Med. 2006;355(16): 1724-1726.

102. Peixoto C, Devicari Cheda JN, Nardi AE, Veras AB, Cardoso A. The effects of dehydroepiandrosterone (DHEA) in the treatment of depression and depressive symptoms in other psychiatric and medical illnesses: a systematic review. Curr. Drug Targets. 2014;15(9):901-914.

103. Arnold JT. DHEA metabolism in prostate: For better or worse? Mol. Cell. Endocrinol. 2009;301(1-2):83-88.

104. Key T, Appleby P, Barnes I, Reeves G, Endogenous H, Breast Cancer Collaborative G. Endogenous sex hormones and breast cancer in postmenopausal women: reanalysis of nine prospective studies. J. Natl. Cancer Inst. 2002;94(8):606-616.

105. Bicanic IA, Postma RM, Sinnema G, et al. Salivary cortisol and dehydroepiandrosterone sulfate in adolescent rape victims with post traumatic stress disorder. Psychoneuroendocrinology. 2013;38(3):408-415.

106. Davidson M, Marwah A, Sawchuk RJ, et al. Safety and pharmacokinetic study with escalating doses of 3-acetyl-7-oxo-dehydroepiandrosterone in healthy male volunteers. Clin. Invest. Med. 2000;23(5):300-310.

107. Bockting CL, Mocking RJ, Lok A, Koeter MW, Schene AH. Therapygenetics: the 5HTTLPR as a biomarker for response to psychological therapy? Mol Psychiatry. 2013;18(7):744-745.

108. Ruhé HG, Khoenkhoen SJ, Ottenhof KW, Koeter MW, Mocking RJ, Schene AH. Longitudinal effects of the SSRI paroxetine on salivary cortisol in Major Depressive Disorder. Psychoneuroendocrinology. 2015;52:261-271.

109. Herane Vives A, De Angel V, Papadopoulos A, et al. The relationship between cortisol, stress and psychiatric illness: New insights using hair analysis. Journal of psychiatric research. 2015;70:38-49.

110. Russo SJ, Murrough JW, Han MH, Charney DS, Nestler EJ. Neurobiology of Resilience. Nat. Neurosci. 2012;15(11):1475-1484.

111. Kamin HS, Kertes DA. Cortisol and DHEA in development and psychopathology. Horm. Behav. 2017;89:69-85.

112. Morris MC, Compas BE, Garber J. Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: a systematic review and meta-analysis. Clin. Psychol. Rev. 2012;32(4):301-315.

113. Rhebergen D, Korten NC, Penninx BW, et al. Hypothalamic-pituitary-adrenal axis activity in older persons with and without a depressive disorder. Psychoneuroendocrinology. 2015;51:341-350.

114. Belvederi Murri M, Pariante C, Mondelli V, et al. HPA axis and aging in depression: Systematic review and meta-analysis. Psychoneuroendocrinology. 2014;41:46-62.

115. Yehuda R, Seckl J. Minireview: Stress-Related Psychiatric Disorders with Low Cortisol Levels: A Metabolic Hypothesis. Endocrinology. 2011;152(12):4496-4503.

116. Frodl T, O’Keane V. How does the brain deal with cumulative stress? A review with focus on developmental stress, HPA axis function and hippocampal structure in humans. Neurobiol. Dis. 2013;52:24-37.

117. Garner B, Phillips LJ, Bendall S, Hetrick SE. Antiglucocorticoid and related treatments for psychosis. The Cochrane database of systematic reviews. 2016(1):Cd006995.

118. Ozbolt LB, Nemeroff CB. HPA Axis Modulation in the Treatment of Mood Disorders. 2013.

119. McAllister-Williams RH, Anderson IM, Finkelmeyer A, et al. Antidepressant augmentation with metyrapone for treatment-resistant depression (the ADD study): a double-blind, randomised, placebo-controlled trial. Lancet Psychiatry. 2016;3(2):117-127.

120. Sanada K, Montero-Marin J, Alda Díez M, et al. Effects of Mindfulness-Based Interventions on Salivary Cortisol in Healthy Adults: A Meta-Analytical Review. Front. Physiol. 2016;7:471.

121. O’Leary K, O’Neill S, Dockray S. A systematic review of the effects of mindfulness interventions on cortisol. J. Health Psychol. 2016;21(9):2108-2121.

122. Fischer S, Strawbridge R, Herane Vives A, Cleare AJ. Cortisol as a predictor of psychological therapy response in depressive disorders: systematic review and meta-analysis. The British Journal of Psychiatry. 2017;210:105-109

123. Hardeveld F, Spijker J, Vreeburg SA, et al. Increased cortisol awakening response was associated with time to recurrence of major depressive disorder. Psychoneuroendocrinology. 2014;50:62-71.

131

124. Verduijn J, Milaneschi Y, Schoevers RA, van Hemert AM, Beekman ATF, Penninx BWJH. Pathophysiology of major depressive disorder: mechanisms involved in etiology are not associated with clinical progression. Translational psychiatry. 2015;5:e649.

125. Kabia FM, Rhebergen D, van Exel E, Stek ML, Comijs HC. The predictive value of cortisol levels on 2-year course of depression in older persons. Psychoneuroendocrinology. 2016;63:320-326.

126. Hough CM, Lindqvist D, Epel ES, et al. Higher serum DHEA concentrations before and after SSRI treatment are associated with remission of major depression. Psychoneuroendocrinology. 2017;77:122-130.

127. Duskova M, Hill M, Bicikova M, et al. The steroid metabolome in men with mood and anxiety disorders. Physiol. Res. 2015;64 Suppl 2:S275-282.

128. Jin RO, Mason S, Mellon SH, et al. Cortisol/DHEA ratio and hippocampal volume: A pilot study in major depression and healthy controls. Psychoneuroendocrinology. 2016;72:139-146.

129. Insel TR. The NIMH Research Domain Criteria (RDoC) Project: precision medicine for psychiatry. Am. J. Psychiatry. 2014;171(4):395-397.

130. Mathews A, MacLeod C. Cognitive approaches to emotion and emotional disorders. Annu. Rev. Psychol. 1994;45:25-50.

131. De Raedt R, Koster EH. Understanding vulnerability for depression from a cognitive neuroscience perspective: A reappraisal of attentional factors and a new conceptual framework. Cogn. Affect. Behav. Neurosci. 2010;10(1):50-70.

132. Leyman L, De Raedt R, Schacht R, Koster EH. Attentional biases for angry faces in unipolar depression. Psychol. Med. 2007;37(3):393-402.

133. Goeleven E, De Raedt R, Baert S, Koster EH. Deficient inhibition of emotional information in depression. J. Affect. Disord. 2006;93(1-3):149-157.

134. Joormann J, Gotlib IH. Selective attention to emotional faces following recovery from depression. J. Abnorm. Psychol. 2007;116(1):80-85.

135. Harmer CJ, Goodwin GM, Cowen PJ. Why do antidepressants take so long to work? A cognitive neuropsychological model of antidepressant drug action. Br. J. Psychiatry. 2009;195(2):102-108.

136. DeRubeis RJ, Siegle GJ, Hollon SD. Cognitive therapy versus medication for depression: treatment outcomes and neural mechanisms. Nat Rev Neurosci. 2008;9(10):788-796.

137. Harmer CJ, O’Sullivan U, Favaron E, et al. Effect of acute antidepressant administration on negative affective bias in depressed patients. Am. J. Psychiatry. 2009;166(10):1178-1184.

138. Pizzagalli DA, Peccoralo LA, Davidson RJ, Cohen JD. Resting anterior cingulate activity and abnormal responses to errors in subjects with elevated depressive symptoms: a 128-channel EEG study. Hum. Brain Mapp. 2006;27(3):185-201.

139. Nolen-Hoeksema S. The role of rumination in depressive disorders and mixed anxiety/depressive symptoms. J. Abnorm. Psychol. 2000;109(3):504-511.

140. Ingram RE. Origins of cognitive vulnerability to depression. Cognit. Ther. Res. 2003;27(1):77-88.

141. Nejad AB, Fossati P, Lemogne C. Self-referential processing, rumination, and cortical midline structures in major depression. Front. Hum. Neurosci. 2013;7:666.

142. Lau MA, Segal ZV, Williams JM. Teasdale’s differential activation hypothesis: implications for mechanisms of depressive relapse and suicidal behaviour. Behav. Res. Ther. 2004;42(9):1001-1017.

143. Phillips ML, Drevets WC, Rauch SL, Lane R. Neurobiology of emotion perception II: Implications for major psychiatric disorders. Biol Psychiatry. 2003;54(5):515-528.

144. Phillips ML, Ladouceur CD, Drevets WC. A neural model of voluntary and automatic emotion regulation: implications for understanding the pathophysiology and neurodevelopment of bipolar disorder. Mol Psychiatry. 2008;13(9):829, 833-857.

145. Mayberg HS. Modulating dysfunctional limbic-cortical circuits in depression: towards development of brain-based algorithms for diagnosis and optimised treatment. Br. Med. Bull. 2003;65:193-207.

146. Pizzagalli DA. Frontocingulate dysfunction in depression: toward biomarkers of treatment response. Neuropsychopharmacology. 2011;36(1):183-206.

147. Surguladze S, Brammer MJ, Keedwell P, et al. A differential pattern of neural response toward sad versus happy facial expressions in major depressive disorder. Biol Psychiatry. 2005;57(3):201-209.

148. Ruhé HG, Booij J, Veltman DJ, Michel MC, Schene AH. Successful pharmacologic treatment of major depressive disorder attenuates amygdala activation to negative facial expressions: a functional magnetic resonance imaging study. The Journal of clinical psychiatry. 2012;73(4):451-459.

149. Groenewold NA, Opmeer EM, de Jonge P, Aleman A, Costafreda SG. Emotional valence modulates brain functional abnormalities in depression: evidence from a meta-analysis of fMRI studies. Neurosci. Biobehav. Rev. 2013;37(2):152-163.

III

132

150. Rive MM, van Rooijen G, Veltman DJ, Phillips ML, Schene AH, Ruhe HG. Neural correlates of dysfunctional emotion regulation in major depressive disorder. A systematic review of neuroimaging studies. Neurosci. Biobehav. Rev. 2013;37(10 Pt 2):2529-2553.

151. Schmaal L, Veltman DJ, van Erp TG, et al. Subcortical brain alterations in major depressive disorder: findings from the ENIGMA Major Depressive Disorder working group. Mol Psychiatry. 2016;21(6):806-812.

152. Schmaal L, Hibar DP, Samann PG, et al. Cortical abnormalities in adults and adolescents with major depression based on brain scans from 20 cohorts worldwide in the ENIGMA Major Depressive Disorder Working Group. Mol Psychiatry. 2016.

153. Frodl TS, Koutsouleris N, Bottlender R, et al. Depression-related variation in brain morphology over 3 years: effects of stress? Archives of general psychiatry. 2008;65(10):1156-1165.

154. Perlis RH, Ostacher MJ, Goldberg JF, et al. Transition to Mania During Treatment of Bipolar Depression. Neuropsychopharmacology. 2010;35(13):2545-2552.

155. Ghaemi SN, Rosenquist KJ, Ko JY, Baldassano CF, Kontos NJ, Baldessarini RJ. Antidepressant Treatment in Bipolar Versus Unipolar Depression. Am. J. Psychiatry. 2004;161(1):163-165.

156. Antidepressant-induced mania and cycle acceleration: a controversy revisited. Am. J. Psychiatry. 1995;152(8):1130-1138.

157. Goodwin GM, Anderson I, Arango C, et al. ECNP consensus meeting. Bipolar depression. Nice, March 2007. Eur. Neuropsychopharmacol. 2008;18(7):535-549.

158. Ghaemi SN, Boiman EE, Goodwin FK. Diagnosing Bipolar Disorder and the Effect of Antidepressants. The Journal of clinical psychiatry. 2000;61(10):804-808.

159. Hirschfeld RMA, Lewis L, Vornik LA. Perceptions and Impact of Bipolar Disorder. The Journal of clinical psychiatry. 2003;64(2):161-174.

160. Phillips ML, Swartz HA. A Critical Appraisal of Neuroimaging Studies of Bipolar Disorder: Toward a New Conceptualization of Underlying Neural Circuitry and a Road Map for Future Research. Am. J. Psychiatry. 2014;171(8):829-843.

161. Price JL, Drevets WC. Neurocircuitry of Mood Disorders. Neuropsychopharmacology. 2009;35(1):192-216.

162. Gotlib IH, Joormann J. Cognition and Depression: Current Status and Future Directions. Ann. Rev. Clin. Psych. 2010;6(1):285-312.

163. Strakowski SM, Adler CM, Almeida J, et al. The functional neuroanatomy of bipolar disorder: a consensus model. Bipolar Disorders. 2012;14(4):313-325.

164. Townsend J, Altshuler LL. Emotion processing and regulation in bipolar disorder: a review. Bipolar Disorders. 2012;14(4):326-339.

165. de Almeida JRC, Phillips ML. Distinguishing between Unipolar Depression and Bipolar Depression: Current and Future Clinical and Neuroimaging Perspectives. Biological Psychiatry. 2013;73(2):111-118.

166. Almeida JRC, Versace A, Hassel S, Kupfer DJ, Phillips ML. Elevated Amygdala Activity to Sad Facial Expressions: A State Marker of Bipolar but Not Unipolar Depression. Biological Psychiatry. 2010;67(5):414-421.

167. Lawrence NS, Williams AM, Surguladze S, et al. Subcortical and ventral prefrontal cortical neural responses to facial expressions distinguish patients with bipolar disorder and major depression. Biological Psychiatry. 2004;55(6):578-587.

168. Diler RS, de Almeida JRC, Ladouceur C, Birmaher B, Axelson D, Phillips M. Neural activity to intense positive versus negative stimuli can help differentiate bipolar disorder from unipolar major depressive disorder in depressed adolescents: A pilot fMRI study. Psychiatry Research: Neuroimaging. 2013;214(3):277-284.

169. Grotegerd D, Stuhrmann A, Kugel H, et al. Amygdala excitability to subliminally presented emotional faces distinguishes unipolar and bipolar depression: An fMRI and pattern classification study. Hum. Brain Mapp. 2013;35(7):2995-3007.

170. Fournier JC, Keener MT, Almeida J, Kronhaus DM, Phillips ML. Amygdala and whole-brain activity to emotional faces distinguishes major depressive disorder and bipolar disorder. Bipolar Disorders. 2013;15(7):741-752.

171. Cerullo MA, Eliassen JC, Smith CT, et al. Bipolar I disorder and major depressive disorder show similar brain activation during depression. Bipolar Disorders. 2014;16(7):703-712.

172. Bertocci MA, Bebko GM, Mullin BC, et al. Abnormal anterior cingulate cortical activity during emotional n-back task performance distinguishes bipolar from unipolar depressed females. Psychol. Med. 2011;42(07):1417-1428.

173. Taylor Tavares JV, Clark L, Cannon DM, Erickson K, Drevets WC, Sahakian BJ. Distinct Profiles of Neurocognitive Function in Unmedicated Unipolar Depression and Bipolar II Depression. Biological Psychiatry. 2007;62(8):917-924.

133

174. Matsubara T, Matsuo K, Nakashima M, et al. Prefrontal activation in response to emotional words in patients with bipolar disorder and major depressive disorder. NeuroImage. 2014;85:489-497.

175. Brühl AB, Kaffenberger T, Herwig U. Serotonergic and Noradrenergic Modulation of Emotion Processing by Single Dose Antidepressants. Neuropsychopharmacology. 2009;35(2):521-533.

176. Fales CL, Barch DM, Rundle MM, et al. Antidepressant treatment normalizes hypoactivity in dorsolateral prefrontal cortex during emotional interference processing in major depression. Journal of Affective Disorders. 2009;112(1-3):206-211.

177. Norbury R, Taylor MJ, Selvaraj S, Murphy SE, Harmer CJ, Cowen PJ. Short-term antidepressant treatment modulates amygdala response to happy faces. Psychopharmacology. 2009;206(2):197-204.

178. Arce E, Simmons AN, Lovero KL, Stein MB, Paulus MP. Escitalopram effects on insula and amygdala BOLD activation during emotional processing. Psychopharmacology. 2007;196(4):661-672.

179. Harmer CJ, Mackay CE, Reid CB, Cowen PJ, Goodwin GM. Antidepressant Drug Treatment Modifies the Neural Processing of Nonconscious Threat Cues. Biological Psychiatry. 2006;59(9):816-820.

180. Diler RS, Ladouceur CD, Segreti A, et al. Neural correlates of treatment response in depressed bipolar adolescents during emotion processing. Brain Imaging and Behavior. 2013;7(2):227-235.

181. Jogia J, Haldane M, Cobb A, Kumari V, Frangou S. Pilot investigation of the changes in cortical activation during facial affect recognition with lamotrigine monotherapy in bipolar disorder. The British Journal of Psychiatry. 2008;192(3):197-201.

182. Haldane M, Jogia J, Cobb A, Kozuch E, Kumari V, Frangou S. Changes in brain activation during working memory and facial recognition tasks in patients with bipolar disorder with Lamotrigine monotherapy. Eur. Neuropsychopharmacol. 2008;18(1):48-54.

183. Bell EC, Willson MC, Wilman AH, Dave S, Silverstone PH. Differential effects of chronic lithium and valproate on brain activation in healthy volunteers. Hum. Psychopharmacol. Clin. Exp. 2005;20(6):415-424.

184. Silverstone PH, Bell EC, Willson MC, Dave S, Wilman AH. Annals of General Psychiatry. 2005;4(1):14.

185. Pavuluri MN, Passarotti AM, Harral EM, Sweeney JA. Enhanced Prefrontal Function With Pharmacotherapy on a Response Inhibition Task in Adolescent Bipolar Disorder. The Journal of clinical psychiatry. 2010;71(11):1526-1534.

186. Pavuluri MN, Passarotti AM, Lu LH, Carbray JA, Sweeney JA. Double-blind randomized trial of risperidone versus divalproex in pediatric bipolar disorder: fMRI outcomes. Psychiatry Research: Neuroimaging. 2011;193(1):28-37.

187. Mourão-Miranda J, Almeida JRC, Hassel S, et al. Pattern recognition analyses of brain activation elicited by happy and neutral faces in unipolar and bipolar depression. Bipolar Disorders. 2012;14(4):451-460.

188. Delvecchio G, Fossati P, Boyer P, et al. Common and distinct neural correlates of emotional processing in Bipolar Disorder and Major Depressive Disorder: A voxel-based meta-analysis of functional magnetic resonance imaging studies. Eur. Neuropsychopharmacol. 2012;22(2):100-113.

189. Hamilton M. A rating scale for depression. Journal of neurology, neurosurgery, and psychiatry. 1960;23.

190. Hamilton MAX. Development of a Rating Scale for Primary Depressive Illness. Br. J. Soc. Clin. Psychol. 1967;6(4):278-296.

191. Johnstone T, van Reekum CM, Urry HL, Kalin NH, Davidson RJ. Failure to regulate: counterproductive recruitment of top-down prefrontal-subcortical circuitry in major depression. J. Neurosci. 2007;27(33):8877-8884.

192. Townsend JD, Torrisi SJ, Lieberman MD, Sugar CA, Bookheimer SY, Altshuler LL. Frontal-Amygdala Connectivity Alterations During Emotion Downregulation in Bipolar I Disorder. Biological Psychiatry. 2013;73(2):127-135.

193. Erk S, Mikschl A, Stier S, et al. Acute and Sustained Effects of Cognitive Emotion Regulation in Major Depression. J. Neurosci. 2010;30(47):15726-15734.

194. Mak AKY, Hu Z-g, Zhang JX, Xiao Z-w, Lee TMC. Neural correlates of regulation of positive and negative emotions: An fMRI study. Neurosci. Lett. 2009;457(2):101-106.

195. Ochsner KN, Bunge SA, Gross JJ, Gabrieli JDE. Rethinking Feelings: An fMRI Study of the Cognitive Regulation of Emotion. J. Cognit. Neurosci. 2002;14(8):1215-1229.

196. Phan KL, Fitzgerald DA, Nathan PJ, Moore GJ, Uhde TW, Tancer ME. Neural substrates for voluntary suppression of negative affect: A functional magnetic resonance imaging study. Biological Psychiatry. 2005;57(3):210-219.

III

134

197. Ohira H, Nomura M, Ichikawa N, et al. Association of neural and physiological responses during voluntary emotion suppression. NeuroImage. 2006;29(3):721-733.

198. Ochsner KN, Ray RD, Cooper JC, et al. For better or for worse: neural systems supporting the cognitive down- and up-regulation of negative emotion. NeuroImage. 2004;23(2):483-499.

199. Maldjian JA, Laurienti PJ, Kraft RA, Burdette JH. An automated method for neuroanatomic and cytoarchitectonic atlas-based interrogation of fMRI data sets. NeuroImage. 2003;19(3):1233-1239.

200. Maldjian JA, Laurienti PJ, Burdette JH. Precentral gyrus discrepancy in electronic versions of the Talairach atlas. NeuroImage. 2004;21(1):450-455.

201. Kanske P, Heissler J, Schönfelder S, Bongers A, Wessa M. How to Regulate Emotion? Neural Networks for Reappraisal and Distraction. Cereb. Cortex. 2010;21(6):1379-1388.

202. Vrtička P, Sander D, Vuilleumier P. Effects of emotion regulation strategy on brain responses to the valence and social content of visual scenes. Neuropsychologia. 2011;49(5):1067-1082.

203. Beauregard M, Lévesque J, Paquette V. 6. Neural basis of conscious and voluntary self-regulation of emotion. Consciousness, Emotional Self-Regulation and the Brain: John Benjamins Publishing Company; 2004:163.

204. Etkin A, Egner T, Kalisch R. Emotional processing in anterior cingulate and medial prefrontal cortex. Trends in Cognitive Sciences. 2011;15(2):85-93.

205. Pizzagalli DA. Frontocingulate Dysfunction in Depression: Toward Biomarkers of Treatment Response. Neuropsychopharmacology. 2010;36(1):183-206.

206. Robinson JL, Monkul ES, Tordesillas-Gutiérrez D, et al. Fronto-limbic circuitry in euthymic bipolar disorder: Evidence for prefrontal hyperactivation. Psychiatry Research: Neuroimaging. 2008;164(2):106-113.

207. Hummer TA, Hulvershorn LA, Karne HS, Gunn AD, Wang Y, Anand A. Emotional Response Inhibition in Bipolar Disorder: A Functional Magnetic Resonance Imaging Study of Trait- and State-Related Abnormalities. Biological Psychiatry. 2013;73(2):136-143.

208. Lee P-S, Chen Y-S, Hsieh J-C, Su T-P, Chen L-F. Distinct neuronal oscillatory responses between patients with bipolar and unipolar disorders: A magnetoencephalographic study. Journal of Affective Disorders. 2010;123(1-3):270-275.

209. Kanske P, Heissler J, Schönfelder S, Wessa M. Neural correlates of emotion regulation deficits in remitted depression: The influence of regulation strategy, habitual regulation use, and emotional valence. NeuroImage. 2012;61(3):686-693.

210. Rottenberg J, Gross JJ, Gotlib IH. Emotion Context Insensitivity in Major Depressive Disorder. J. Abnorm. Psychol. 2005;114(4):627-639.

211. Kelly RE, Mansell W, Wood AM, Alatiq Y, Dodd A, Searson R. Extreme positive and negative appraisals of activated states interact to discriminate bipolar disorder from unipolar depression and non-clinical controls. Journal of Affective Disorders. 2011;134(1-3):438-443.

212. Johnson SL, McKenzie G, McMurrich S. Ruminative Responses to Negative and Positive Affect Among Students Diagnosed with Bipolar Disorder and Major Depressive Disorder. Cognit. Ther. Res. 2007;32(5):702-713.

213. Etkin A, Egner T, Peraza DM, Kandel ER, Hirsch J. Resolving Emotional Conflict: A Role for the Rostral Anterior Cingulate Cortex in Modulating Activity in the Amygdala. Neuron. 2006;51(6):871-882.

214. Sachs GS, Nierenberg AA, Calabrese JR, et al. Effectiveness of Adjunctive Antidepressant Treatment for Bipolar Depression. New Engl. J. Med. 2007;356(17):1711-1722.

215. Scott J. Cognitive-behavioural therapy for severe and recurrent bipolar disorders: Randomised controlled trial. The British Journal of Psychiatry. 2006;188(4):313-320.

216. Strakowski SM, Adler CM, Holland SK, Mills N, DelBello MP. A Preliminary fMRI Study of Sustained Attention in Euthymic, Unmedicated Bipolar Disorder. Neuropsychopharmacology. 2004;29(9):1734-1740.

217. Beblo T, Sinnamon G, Baune BT. Specifying the Neuropsychology of Affective Disorders: Clinical, Demographic and Neurobiological Factors. Neuropsychol. Rev. 2011;21(4):337-359.

218. Mur M, Portella MJ, Martinez-Aran A, Pifarre J, Vieta E. Influence of Clinical and Neuropsychological Variables on the Psychosocial and Occupational Outcome of Remitted Bipolar Patients. Psychopathology. 2009;42(3):148-156.

219. Baune BT, Li X, Beblo T. Short- and long-term relationships between neurocognitive performance and general function in bipolar disorder. J. Clin. Exp. Neuropsychol. 2013;35(7):759-774.

220. Goodwin GM, Martinez-Aran A, Glahn DC, Vieta E. Cognitive impairment in bipolar disorder: Neurodevelopment or neurodegeneration? An ECNP expert meeting report. Eur. Neuropsychopharmacol. 2008;18(11):787-793.

135

221. Daniel BD, Montali A, Gerra ML, et al. Cognitive Impairment and its Associations with the Path of Illness in Affective Disorders. J. Psychiatr. Pract. 2013;19(4):275-287.

222. Gong Q, He Y. Depression, neuroimaging and connectomics: a selective overview. Biol Psychiatry. 2015;77(3):223-235.

223. Mulders PC, van Eijndhoven PF, Schene AH, Beckmann CF, Tendolkar I. Resting-state functional connectivity in major depressive disorder: A review. Neurosci. Biobehav. Rev. 2015;56:330-344.

224. Kaiser RH, Andrews-Hanna JR, Wager TD, Pizzagalli DA. Large-Scale Network Dysfunction in Major Depressive Disorder: A Meta-analysis of Resting-State Functional Connectivity. JAMA Psychiatry. 2015;72(6):603-611.

225. Arnone D, Mumuni AN, Jauhar S, Condon B, Cavanagh J. Indirect evidence of selective glial involvement in glutamate-based mechanisms of mood regulation in depression: meta-analysis of absolute prefrontal neuro-metabolic concentrations. Eur. Neuropsychopharmacol. 2015;25(8):1109-1117.

226. Lener MS, Niciu MJ, Ballard ED, et al. Glutamate and Gamma-Aminobutyric Acid Systems in the Pathophysiology of Major Depression and Antidepressant Response to Ketamine. Biological Psychiatry.

227. Goodkind M, Eickhoff SB, Oathes DJ, et al. Identification of a common neurobiological substrate for mental illness. JAMA Psychiatry. 2015;72(4):305-315.

228. Servaas MN, Riese H, Renken RJ, et al. Associations between Daily Affective Instability and Connectomics in Functional Subnetworks in Remitted Patients with Recurrent Major Depressive Disorder. Neuropsychopharmacology. 2017.

229. Eklund A, Nichols TE, Knutsson H. Cluster failure: Why fMRI inferences for spatial extent have inflated false-positive rates. Proceedings of the National Academy of Sciences of the United States of America. 2016;113(28):7900-7905.

230. Fischer AS, Keller CJ, Etkin A. The Clinical Applicability of Functional Connectivity in Depression: Pathways Toward More Targeted Intervention. Biological Psychiatry: Cognitive Neuroscience and Neuroimaging. 2016;1(3): 262-270.

231. Lener MS, Iosifescu DV. In pursuit of neuroimaging biomarkers to guide treatment selection in major depressive disorder: a review of the literature. Ann. N. Y. Acad. Sci. 2015;1344(1):50-65.

232. van Waarde JA, Scholte HS, van Oudheusden LJB, Verwey B, Denys D, van Wingen GA. A functional MRI marker may predict the outcome of electroconvulsive therapy in severe and treatment-resistant depression. Mol Psychiatry. 2015;20(5):609-614.

233. Schmaal L, Marquand AF, Rhebergen D, et al. Predicting the Naturalistic Course of Major Depressive Disorder Using Clinical and Multimodal Neuroimaging Information: A Multivariate Pattern Recognition Study. Biological Psychiatry. 2015;78(4):278-286.

234. Rive MM, Redlich R, Schmaal L, et al. Distinguishing medication-free subjects with unipolar disorder from subjects with bipolar disorder: state matters. Bipolar Disord. 2016;18(7):612-623.

235. Xia M, He Y. Functional connectomics from a “big data” perspective. NeuroImage. 2017.

236. Crossley NA, Fox PT, Bullmore ET. Meta-connectomics: human brain network and connectivity meta-analyses. Psychol. Med. 2016;46(5):897-907.

237. Mocking RJ, Patrick Pflanz C, Pringle A, et al. Effects of short-term varenicline administration on emotional and cognitive processing in healthy, non-smoking adults: a randomized, double-blind, study. Neuropsychopharmacology. 2013;38(3):476-484.

238. Horder J, Browning M, Di Simplicio M, Cowen PJ, Harmer CJ. Effects of 7 days of treatment with the cannabinoid type 1 receptor antagonist, rimonabant, on emotional processing. J Psychopharmacol. 2012;26(1):125-132.

239. Mocking RJ, Figueroa CA, Rive MM, et al. Vulnerability for new episodes in recurrent major depressive disorder: protocol for the longitudinal DELTA-neuroimaging cohort study. BMJ Open. 2016;6(3):e009510.

III