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MRI research progress of brain function and structure in patients with major depressive disorder before and after treatment
LI Haidong  WANG Jun  NIU Jinliang 

Cite this article as: Li HD, Wang J, Niu JL. MRI research progress of brain function and structure in patients with major depressive disorder before and after treatment[J]. Chin J Magn Reson Imaging, 2022, 13(3): 143-146. DOI:10.12015/issn.1674-8034.2022.03.035.


[Abstract] Major depressive disorder (MDD) is a psychiatric disorder that is caused by varieties of factors, which can result in symptoms such as upset and cognitive impairment. Different changes in brain function and structure exist before and after antidepressant treatment. MRI can further identify the neuropathophysiological mechanisms associated with the symptoms of MDD. Recent drug-naive MDD studies have shown decreased regional brain activity in prefrontal cortex, cingulate, precuneus, hippocampus and increased functional connectivity in default mode network (DMN), central executive network (CEN), salience network (SN). These studies also exhibite the reduction of gray matter volume and disruption of white matter simultaneously. Post-treatment studies display increased brain activity in partial brain regions, which also indicate the normalization in DMN, CEN, SN, gray matter volume and white matter structure. This paper reviews the effects of major depressive disorder before and after antidepressant treatment from the perspective of functional and structural MRI to provide objective reference information for early diagnosis and curative effect evaluation.
[Keywords] major depressive disorder;magnetic resonance imaging;brain structure;brain function;mechanism;antidepressant therapy;imaging marker

LI Haidong1   WANG Jun2   NIU Jinliang2*  

1 College of Medical Imaging, Shanxi Medical University, Taiyuan 030001, China

2 Department of Magnetic Resonance Imaging, the Second Hospital of Shanxi Medical University, Taiyuan 030001, China

Niu JL, E-mail: sxlscjy@163.com

Conflicts of interest   None.

Received  2021-11-25
Accepted  2022-03-14
DOI: 10.12015/issn.1674-8034.2022.03.035
Cite this article as: Li HD, Wang J, Niu JL. MRI research progress of brain function and structure in patients with major depressive disorder before and after treatment[J]. Chin J Magn Reson Imaging, 2022, 13(3): 143-146.DOI:10.12015/issn.1674-8034.2022.03.035

[1]
Lim SS, Vos T, Flaxman AD, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010[J]. Lancet, 2012, 380(9859): 2224-2260. DOI: 10.1016/S0140-6736(12)61766-8.
[2]
Spellman T, Liston C. Toward circuit mechanisms of pathophysiology in depression[J]. Am J Psychiatry, 2020, 177(5): 381-390. DOI: 10.1176/appi.ajp.2020.20030280.
[3]
Shao XJ, Zhu G. Associations among monoamine neurotransmitter pathways, personality traits, and major depressive disorder[J]. Front Psychiatry, 2020, 11: 381. DOI: 10.3389/fpsyt.2020.00381.
[4]
Dwyer JB, Aftab A, Radhakrishnan R, et al. Hormonal treatments for major depressive disorder: state of the art[J]. Am J Psychiatry, 2020, 177(8): 686-705. DOI: 10.1176/appi.ajp.2020.19080848.
[5]
Suda K, Matsuda K. How microbes affect depression: underlying mechanisms via the gut-brain axis and the modulating role of probiotics[J]. Int J Mol Sci, 2022, 23(3): 1172. DOI: 10.3390/ijms23031172.
[6]
Wiebenga JXM, Heering HD, Eikelenboom M, et al. Associations of three major physiological stress systems with suicidal ideation and suicide attempts in patients with a depressive and/or anxiety disorder[J]. Brain Behav Immun, 2022, 102: 195-205. DOI: 10.1016/j.bbi.2022.02.021.
[7]
Wang L, Li K, Zhang Q, et al. Short-term effects of escitalopram on regional brain function in first-episode drug-naive patients with major depressive disorder assessed by resting-state functional magnetic resonance imaging[J]. Psychol Med, 2014, 44(7): 1417-1426. DOI: 10.1017/S0033291713002031.
[8]
Jiang XW, Fu SN, Yin ZY, et al. Common and distinct neural activities in frontoparietal network in first-episode bipolar disorder and major depressive disorder: preliminary findings from a follow-up resting state fMRI study[J]. J Affect Disord, 2020, 260: 653-659. DOI: 10.1016/j.jad.2019.09.063.
[9]
Zhang ZJ, Chen YY, Wei W, et al. Changes in regional homogeneity of medication-free major depressive disorder patients with different onset ages[J]. Front Psychiatry, 2021, 12: 713614. DOI: 10.3389/fpsyt.2021.713614.
[10]
Cheng Y, Xu J, Arnone D, et al. Resting-state brain alteration after a single dose of SSRI administration predicts 8-week remission of patients with major depressive disorder[J]. Psychol Med, 2017, 47(3): 438-450. DOI: 10.1017/S0033291716002440.
[11]
Wang M, Ju YM, Lu XW, et al. Longitudinal changes of amplitude of low-frequency fluctuations in MDD patients: a 6-month follow-up resting-state functional magnetic resonance imaging study[J]. J Affect Disord, 2020, 276: 411-417. DOI: 10.1016/j.jad.2020.07.067.
[12]
Lan MJ, Rizk MM, Pantazatos SP, et al. Resting-state amplitude of low-frequency fluctuation is associated with suicidal ideation[J]. Depress Anxiety, 2019, 36(5): 433-441. DOI: 10.1002/da.22888.
[13]
Liu PH, Tu HW, Zhang AX, et al. Brain functional alterations in MDD patients with somatic symptoms: a resting-state fMRI study[J]. J Affect Disord, 2021, 295: 788-796. DOI: 10.1016/j.jad.2021.08.143.
[14]
Scalabrini A, Vai B, Poletti S, et al. All roads lead to the default-mode network-global source of DMN abnormalities in major depressive disorder[J]. Neuropsychopharmacology, 2020, 45(12): 2058-2069. DOI: 10.1038/s41386-020-0785-x.
[15]
Li YL, Dai X, Wu HW, et al. Establishment of effective biomarkers for depression diagnosis with fusion of multiple resting-state connectivity measures[J]. Front Neurosci, 2021, 15: 729958. DOI: 10.3389/fnins.2021.729958.
[16]
Alders GL, Davis AD, MacQueen G, et al. Reduced accuracy accompanied by reduced neural activity during the performance of an emotional conflict task by unmedicated patients with major depression: a CAN-BIND fMRI study[J]. J Affect Disord, 2019, 257: 765-773. DOI: 10.1016/j.jad.2019.07.037.
[17]
Miller JM, Schneck N, Siegle GJ, et al. fMRI response to negative words and SSRI treatment outcome in major depressive disorder: a preliminary study[J]. Psychiatry Res Neuroimaging, 2013, 214(3): 296-305. DOI: 10.1016/j.pscychresns.2013.08.001.
[18]
Lai CH, Wu YT. Frontal regional homogeneity increased and temporal regional homogeneity decreased after remission of first-episode drug-naïve major depressive disorder with panic disorder patients under duloxetine therapy for 6 weeks[J]. J Affect Disord, 2012, 136(3): 453-458. DOI: 10.1016/j.jad.2011.11.004.
[19]
Yang CX, Zhang AX, Jia AX, et al. Identify abnormalities in resting-state brain function between first-episode, drug-naive major depressive disorder and remitted individuals: a 3-year retrospective study[J]. Neuroreport, 2018, 29(11): 907-916. DOI: 10.1097/WNR.0000000000001054.
[20]
Zhou M, Hu XY, Lu L, et al. Intrinsic cerebral activity at resting state in adults with major depressive disorder: a meta-analysis[J]. Prog Neuro Psychopharmacol Biol Psychiatry, 2017, 75: 157-164. DOI: 10.1016/j.pnpbp.2017.02.001.
[21]
Li BJ, Liu L, Friston KJ, et al. A treatment-resistant default mode subnetwork in major depression[J]. Biol Psychiatry, 2013, 74(1): 48-54. DOI: 10.1016/j.biopsych.2012.11.007.
[22]
Sahib AK, Loureiro JR, Vasavada M, et al. Modulation of the functional connectome in major depressive disorder by ketamine therapy[J]. Psychol Med, 2020: 1-10. DOI: 10.1017/s0033291720004560.
[23]
Li L, Su YN, Wu YK, et al. Eight-week antidepressant treatment reduces functional connectivity in first-episode drug-naïve patients with major depressive disorder[J]. Hum Brain Mapp, 2021, 42(8): 2593-2605. DOI: 10.1002/hbm.25391.
[24]
Chin Fatt CR, Jha MK, Cooper CM, et al. Effect of intrinsic patterns of functional brain connectivity in moderating antidepressant treatment response in major depression[J]. Am J Psychiatry, 2020, 177(2): 143-154. DOI: 10.1176/appi.ajp.2019.18070870.
[25]
Mkrtchian A, Evans JW, Kraus C, et al. Ketamine modulates fronto-striatal circuitry in depressed and healthy individuals[J]. Mol Psychiatry, 2021, 26(7): 3292-3301. DOI: 10.1038/s41380-020-00878-1.
[26]
Karim HT, Andreescu C, Tudorascu D, et al. Intrinsic functional connectivity in late-life depression: trajectories over the course of pharmacotherapy in remitters and non-remitters[J]. Mol Psychiatry, 2017, 22(3): 450-457. DOI: 10.1038/mp.2016.55.
[27]
Williams RJ, Brown EC, Clark DL, et al. Early post-treatment blood oxygenation level-dependent responses to emotion processing associated with clinical response to pharmacological treatment in major depressive disorder[J]. Brain Behav, 2021, 11(8): e2287. DOI: 10.1002/brb3.2287.
[28]
Frodl T, Scheuerecker J, Schoepf V, et al. Different effects of mirtazapine and venlafaxine on brain activation[J]. J Clin Psychiatry, 2011, 72(4): 448-457. DOI: 10.4088/jcp.09m05393blu.
[29]
Reed JL, Nugent AC, Furey ML, et al. Effects of ketamine on brain activity during emotional processing: differential findings in depressed versus healthy control participants[J]. Biol Psychiatry Cogn Neurosci Neuroimaging, 2019, 4(7): 610-618. DOI: 10.1016/j.bpsc.2019.01.005.
[30]
Seminowicz DA, Mayberg HS, McIntosh AR, et al. Limbic-frontal circuitry in major depression: a path modeling metanalysis[J]. NeuroImage, 2004, 22(1): 409-418. DOI: 10.1016/j.neuroimage.2004.01.015.
[31]
Zhou HX, Chen X, Shen YQ, et al. Rumination and the default mode network: Meta-analysis of brain imaging studies and implications for depression[J]. NeuroImage, 2020, 206: 116287. DOI: 10.1016/j.neuroimage.2019.116287.
[32]
Yin JB, Liang SH, Li F, et al. dmPFC-vlPAG projection neurons contribute to pain threshold maintenance and antianxiety behaviors[J]. J Clin Invest, 2020, 130(12): 6555-6570. DOI: 10.1172/JCI127607.
[33]
Qiu J, Wang BX, Wang L, et al. Research on regional homogeneity of resting state functional magnetic resonance imaging in first-episode depressive disorder patients[J]. Chin J Magn Reson Imaging, 2020, 11(9): 721-725. DOI: 10.12015/issn.1674-8034.2020.09.001.
[34]
Köhler CA, Carvalho AF, Alves GS, et al. Autobiographical memory disturbances in depression: a novel therapeutic target?[J]. Neural Plast, 2015, 2015: 759139. DOI: 10.1155/2015/759139.
[35]
Zhang Q, Hong S, Cao J, et al. Hippocampal subfield volumes in major depressive disorder adolescents with a history of suicide attempt[J]. Biomed Res Int, 2021, 2021: 5524846. DOI: 10.1155/2021/5524846.
[36]
Blier P, Mansari ME. Serotonin and beyond: therapeutics for major depression[J]. Philos Trans R Soc Lond B Biol Sci, 2013, 368(1615): 20120536. DOI: 10.1098/rstb.2012.0536.
[37]
Duman RS, Aghajanian GK, Sanacora G, et al. Synaptic plasticity and depression: new insights from stress and rapid-acting antidepressants[J]. Nat Med, 2016, 22(3): 238-249. DOI: 10.1038/nm.4050.
[38]
Marques Périco C, Dickstein DP, Farrow TFD, et al. Common and distinct patterns of grey-matter volume alteration in major depression and bipolar disorder: evidence from voxel-based meta-analysis. Mol Psychiatry, 2017, 22(10):1455-1463. DOI: 10.1038/mp.2016.72.
[39]
Li Q, Zhao Y, Chen Z, et al. Meta-analysis of cortical thickness abnormalities in medication-free patients with major depressive disorder. Neuropsychopharmacology, 2020, 45(4):703-712. DOI: 10.1038/s41386-019-0563-9.
[40]
Yu MC, Cullen N, Linn KA, et al. Structural brain measures linked to clinical phenotypes in major depression replicate across clinical centres[J]. Mol Psychiatry, 2021, 26(7): 2764-2775. DOI: 10.1038/s41380-021-01039-8.
[41]
van Velzen LS, Kelly S, Isaev D, et al. White matter disturbances in major depressive disorder: a coordinated analysis across 20 international cohorts in the ENIGMA MDD working group[J]. Mol Psychiatry, 2020, 25(7): 1511-1525. DOI: 10.1038/s41380-019-0477-2.
[42]
Jiang J, Zhao YJ, Hu XY, et al. Microstructural brain abnormalities in medication-free patients with major depressive disorder: a systematic review and meta-analysis of diffusion tensor imaging[J]. J Psychiatry Neurosci, 2017, 42(3): 150-163. DOI: 10.1503/jpn.150341.
[43]
Wang Y, Zhao T, Xie J, et al. The study of white matter micro-structures mediating onset age and the severity of depressive disorder based on DTI[J]. Chin J Magn Reson Imaging, 2021, 12(6): 1-4, 15. DOI: 10.12015/issn.1674-8034.2021.06.001.
[44]
Rutland JW, Brown S, Verma G, et al. Hippocampal subfield-specific connectivity findings in major depressive disorder: a 7 Tesla diffusion MRI study[J]. J Psychiatr Res, 2019, 111: 186-192. DOI: 10.1016/j.jpsychires.2019.02.008.
[45]
Zarate-Garza PP, Ortega-Balderas JA, Ontiveros-Sanchez de la Barquera JA, et al. Hippocampal volume as treatment predictor in antidepressant naïve patients with major depressive disorder[J]. J Psychiatr Res, 2021, 140: 323-328. DOI: 10.1016/j.jpsychires.2021.06.008.
[46]
Bartlett EA, DeLorenzo C, Sharma P, et al. Pretreatment and early-treatment cortical thickness is associated with SSRI treatment response in major depressive disorder[J]. Neuropsychopharmacology, 2018, 43(11): 2221-2230. DOI: 10.1038/s41386-018-0122-9.
[47]
Kraus C, Seiger R, Pfabigan DM, et al. Hippocampal subfields in acute and remitted depression-an ultra-high field magnetic resonance imaging study[J]. Int J Neuropsychopharmacol, 2019, 22(8): 513-522. DOI: 10.1093/ijnp/pyz030.
[48]
Voineskos AN, Mulsant BH, Dickie EW, et al. Effects of antipsychotic medication on brain structure in patients with major depressive disorder and psychotic features: neuroimaging findings in the context of a randomized placebo-controlled clinical trial[J]. JAMA Psychiatry, 2020, 77(7): 674-683. DOI: 10.1001/jamapsychiatry.2020.0036.
[49]
Sydnor VJ, Lyall AE, Cetin-Karayumak S, et al. Studying pre-treatment and ketamine-induced changes in white matter microstructure in the context of ketamine's antidepressant effects[J]. Transl Psychiatry, 2020, 10(1): 432. DOI: 10.1038/s41398-020-01122-8.
[50]
Melloni EMT, Poletti S, Dallaspezia S, et al. Changes of white matter microstructure after successful treatment of bipolar depression[J]. J Affect Disord, 2020, 274(1): 1049-1056. DOI: 10.1016/j.jad.2020.05.146.
[51]
Narr KL, Bilder RM, Toga AW, et al. Mapping cortical thickness and gray matter concentration in first episode schizophrenia[J]. Cereb Cortex, 2005, 15(6): 708-719. DOI: 10.1093/cercor/bhh172.
[52]
Cotter D, MacKay D, Chana G, et al. Reduced neuronal size and glial cell density in area 9 of the dorsolateral prefrontal cortex in subjects with major depressive disorder[J]. Cereb Cortex, 2002, 12(4): 386-394. DOI: 10.1093/cercor/12.4.386.

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