抑郁障碍患者楔前叶功能连接与抗抑郁药物早期疗效的相关性

背景 默认网络内楔前叶功能活动与抗抑郁药物的疗效有关。然而,楔前叶功能网络与抗抑郁药物早期疗效的关系仍不清楚。 目的 探索抑郁障碍患者楔前叶功能连接（FC）与抗抑郁药物早期疗效的关系,以期寻找预测抗抑郁药物早期疗效的神经生物标志物。 方法 连续纳入2017年7月—2019年2月在四川大学华西医院心理卫生中心就诊的、符合《精神障碍诊断与统计手册（第5版）》（DSM-5）诊断标准的47例抑郁障碍患者。采集患者基线期静息态功能磁共振（rs-fMRI）数据及临床信息。患者接受2周抗抑郁药物治疗,根据治疗2周时16项抑郁症状快速自评量表（QIDS-SR16）评分减分率是否≥20%,将患者分为早期改善组（ n=27）和未改善组（ n=20）。以双侧楔前叶为种子点,计算楔前叶与全脑FC值,比较两组基线期楔前叶FC的差异。采用Pearson相关分析考查差异有统计学意义的脑区的FC值与QIDS-SR16评分及其减分率之间的相关性。 结果 早期改善组左侧楔前叶与左侧中央前回的FC值、右侧楔前叶与右侧梭状回的FC值均高于未改善组（GRF校正, P<0.01）。抑郁障碍患者左侧楔前叶与左侧中央前回的FC值、右侧楔前叶与右侧梭状回的FC值与QIDS-SR16总评分减分率均呈正相关（ r=0.475、0.297, P均<0.05）。 结论 基线期较低的左侧楔前叶与左侧中央前回、右侧楔前叶与右侧梭状回的FC与较差的抗抑郁药物早期疗效有关,楔前叶FC可能是预测抗抑郁药物早期疗效的潜在指标。     

Interaction of serotonin-related genes affects short-term antidepressant response in major depressive disorder

Background

Four serotonin-related genes including guanine nucleotide binding protein beta polypeptide 3 (GNB3), 5-hydroxytryptamine receptor 1A (HTR1A; serotonin receptor 1A), 5-hydroxytryptamine receptor 2A (HTR2A; serotonin receptor 2A), and solute carrier family 6 member 4 (SLC6A4; serotonin neurotransmitter transporter) have been suggested to be candidate genes for influencing antidepressant treatment outcome. The aim of this study was to explore whether interaction among these genes could contribute to the pharmacogenomics of short-term antidepressant response in a Taiwanese population with major depressive disorder (MDD).

Methods

Included in this study were 101 MDD patients who were treated with antidepressants, 35 of whom were rapid responders and 66 non-responders after 2 weeks of treatment. We genotyped four single nucleotide polymorphisms (SNPs), including GNB3 rs5443 (C825T), HTR1A rs6295 (C-1019G), HTR2A rs6311 (T102C), and SLC6A4 rs25533, and employed the generalized multifactor dimensionality reduction (GMDR) method to investigate gene–gene interactions.

Results

Single-locus analyses showed the GNB3 rs5443 polymorphism to be associated with short-term antidepressant treatment outcome (P-value = 0.029). We did not correct for multiple testing in these multiple exploratory analyses. Finally, the GMDR approach identified a significant gene–gene interaction (P-value = 0.025) involving GNB3 and HTR2A, as well as a significant 3-locus model (P-value = 0.015) among GNB3, HTR2A, and SLC6A4.

Conclusions

These results support the hypothesis that GNB3, HTR2A, and SLC6A4 may play a role in the outcome of short-term antidepressant treatment for MDD in an interactive manner. Future research with independent replication using large sample sizes is needed to confirm the functions of the candidate genes identified in this study as being involved in short-term antidepressant treatment response.     

Diagnosis and treatment of major depressive disorder

Major depressive disorder is a common illness, particularly in patients with medical and neurologic conditions. This article summarizes current data on the epidemiology, diagnosis, and treatment of major depression, with special emphasis on the diagnosis and treatment of depression in medical and neurologic patients. We reviewed the role of pharmacotherapies, psychotherapies, somatic treatments, and alternative remedies and we included practical advice for clinician regarding the timing and sequence of these treatments, the role of standardized depression scales, and the criteria for referrals to specialty consultants.     

Aripiprazole augmentation versus antidepressant switching for patients with major depressive disorder: A 6-week,randomized, rater-blinded,prospective study

No study has directly compared the efficacy and tolerability of aripiprazole augmentation (AA) and antidepressant switching (SW) in patients with major depressive disorder (MDD). This is the first 6-week, randomized, rater-blinded, direct comparison study between AA and SW in outpatients. An inadequate response to antidepressants was defined as a total score ≥14 on the Hamilton Depression Rating Scale-item 17 (HDRS-17) despite adequate antidepressant dosage for at least 6 weeks in the current depressive episode. The primary endpoint was change in the total score of the Montgomery–Åsberg Depression Rating Scale (MADRS) from baseline to the end of treatment. Secondary efficacy measures included the response and remission rates as priori defined at the end of treatment: changes in total scores of the HDRS-17, Iowa Fatigue Scale (IFS), and Sheehan Disability Scale (SDS) from baseline to the end of treatment and the proportion of patients who scored 1 or 2 on the Clinical Global Impression-Improvement Score (CGI-I) at the end of treatment. Tolerability was assessed with the Barnes Akathisia Rating Scale (BARS) and Arizona Sexual dysfunction scale (ASEX), and the numbers of adverse events were compared between the two groups. A total of 101 patients were randomized to either AA (n = 52) or SW (n = 49). The mean change in the MADRS score from baseline was significantly higher in the AA, with a difference in magnitude of −8.7 (p < 0.0001). The intergroup difference was first evident in week 2. The numbers of responders (p = 0.0086) and remitters (p = 0.0005) were also significantly higher in the AA (60% and 54%, respectively) compared with the SW (32.6% and 19.6%, respectively). On most secondary endpoints, AA showed better clinical outcomes compared to SW. The tolerability profiles were comparable between the two groups. Overall, AA yielded potentially beneficial clinical outcomes compared to SW. Given the methodological shortcomings of the present study, adequately powered, more rigorously controlled clinical trials are strongly warranted to confirm the present findings.     

Topological network mechanisms of clinical response to antidepressant treatment in drug-naive major depressive disorder

AimThere is rapidly increasing evidence that remission of MDD is associated with substantial changes in functional brain connectivity. These New data have provided a holistic view on the mechanism of antidepressants on multiple levels that goes beyond their conventional effects on neurotransmitters.MethodThe study was approved by the Local Ethics Committee of Istanbul Medipol University (10840098-604.01.01-E.65129) and followed the Helsinki Declaration principles. In our study, we have evaluated the effect of six weeks of treatment with antidepressants (escitalopram and duloxetine), and tested the underlying brain functional connectivity through a Graph analysis approach in a well-defined first-episode, drug-naive, and non-comorbid population with MDD.ResultsBeyond indicating that there was a significant correlation between the antidepressant response and topological characteristics of the brain, our results suggested that global rather than regional network alterations may be implicated in the antidepressant effect.ConclusionDespite the small-sample size and non-controlled study design, our study provides important and relevant clinical data regarding the underlying mechanisms of the antidepressants on topological dynamics in the human brain.     

抑郁症患者焦虑/躯体化症状早期的变化与氟西汀疗效的相关性研究

目的探讨抑郁症患者焦虑／躯体化症状的早期变化对氟西汀抗抑郁治疗达症状缓解的预测作用。方法对103例重症抑郁患者给予氟西汀治疗6w,剂量固定于20 mg／d,于治疗前及治疗后的第1、2、4、6w末用汉密顿抑郁量表17项(HAMD-17)评定临床症状,其中焦虑／躯体化因子分用来评定焦虑／躯体化症状。结果治疗6w末103例患者中32例(31．1％)达到症状缓解标准,71例(68．9 ％)未达到症状缓解标准。早期HAMD-17中焦虑／躯体化因子分及胃肠道症状条目分的变化与症状缓解存在正相关,而该因子中其余条目的变化与症状缓解不相关。结论HAMD-17中焦虑／躯体化因子分及胃肠道症状有关的条目分早期改善可能是氟西汀治疗后症状能基本缓解的预测因子。     

艾司西酞普兰治疗后抑郁症患者功能磁共振影像学改变的研究进展

本文目的是探讨抑郁症患者接受艾司西酞普兰治疗前后大脑功能磁共振激活改变.功能磁共振研究显示,治疗前,抑郁症患者前额叶、扣带回和纹状体等脑区的活动存在异常,前扣带回、背外侧前额叶、丘脑异常激活可预测艾司西酞普兰的疗效.经艾司西酞普兰治疗后,患者部分脑区恢复正常,且脑区激活的改变与症状的改善具有相关性.本文对抑郁症患者治疗...     

The 'resting-state hypothesis' of major depressive disorder-a translational subcortical-cortical framework for a system disorder

Major depressive disorder (MDD) has traditionally been characterized by various psychological symptoms, involvement of diverse functional systems (e.g., somatic, affect, cognition, reward, etc.), and with progress in neuroscience, an increasing number of brain regions. This has led to the general assumption that MDD is a stress–responsive brain ‘system disorder’ where either one or several alterations infiltrate a large number of functional systems in the brain that control the organism's somatic, affective, and cognitive life. However, while the effects or consequences of the abnormal changes in the functional systems of, for instance affect, cognition or reward have been investigated extensively, the underlying core mechanism(s) underlying MDD remain unknown. Hypotheses are proliferating rapidly, though. Based on recent findings, we will entertain an abnormality in the resting-state activity in MDD to be a core feature. Based on both animal and human data, we hypothesize that abnormal resting-state activity levels may impact stimulus-induced neural activity in medially situated core systems for self-representation as well as external stimulus (especially stress, specifically separation distress) interactions. Moreover, due to nested hierarchy between subcortical and cortical regions, we assume ‘highjacking’ of higher cortical affective and cognitive functions by lower subcortical primary-process emotional systems. This may account for the predominance of negative affect in somatic and cognitive functional system operations with the consecutive generation of the diverse symptoms in MDD. We will here focus on the neuroanatomical and biochemical basis of resting-state abnormalities in MDD including their linkage to the diverse psychopathological symptoms in depression. However, our ‘resting-state hypothesis’ may go well beyond that by being sufficiently precise to be linked to genetic, social, immunological, and endocrine dimensions and hypotheses as well as to clinical dimensions like endophenotypes and various diagnostic-prognostic biomarkers. Taken together, our ‘resting-state hypothesis’ may be considered a first tentative framework for MDD that integrates translational data, the various dimensions, and subcortical–cortical systems while at the same time providing the link to the clinical level of symptoms, endophenotypes and biomarkers.     

Non response at week 4 as clinically useful indicator for antidepressant combination in major depressive disorder. A sequential RCT

We aimed to compare the efficacy and tolerability of mirtazapine versus SSRIs and to assess whether “non-response at week 4” may be a clinical indicator for combining mirtazapine and SSRIs for subsequent treatment. One-hundred fifty-four outpatients with MDD were randomized to receive mirtazapine or SSRIs in step I (4 weeks). Non-responders in step I were randomly assigned to either mirtazapine or SSRIs monotherapy or their combination in step IIa while responders in step I continued the same monotherapy in step IIb for 4 weeks. In step I, mirtazapine showed significantly faster improvement as shown by higher remission rate at week 2 with NNT = 8 compared to SSRIs. Somnolence rate was higher in mirtazapine and nausea rate was higher in SSRIs. In step IIa, combination therapy showed a more favorable time course than SSRIs monotherapy. For subjects taking SSRIs in step I, combination therapy showed significant better improvement in the Hamilton Depression Rating (HAM-D) score both at week 6 (p = 0.006) and 8 (p = 0.013) than SSRIs monotherapy. About 80% of responders at week 4 could reach remission at week 8 and 64% of non-responders could not reach remission at week 8 for patients who continued monotherapy. When mirtazapine was added on for SSRIs non-responders at week 4, the remission rate increased by 5% and HAM-D score improved by 4 points. While for mirtazapine non-responders, SSRIs add-on was not equally effective.Mirtazapine may provide a faster improvement and “non-response at week 4” may be indicator to mirtazapine add-on for patients receiving SSRIs.     

抑郁症的睡眠质量及其相关影响因素

目的了解保定市抑郁症睡眠质量特点及其相关影响因素。方法采用多阶段分层整群抽样方法随机抽取≥18周岁的人群，共10073名，用扩展的一般健康问卷（GHQ-12）将调查对象分为高、中、低危险组，以美国精神障碍诊断与统计手册-第四版（DSM—Ⅳ）轴Ⅰ障碍定式临床检查病人版（SCID—L／P）对调查对象进行抑郁症的诊断。以匹兹堡睡眠质量指数（PSQI）评定睡眠质量。结果8773人完成了TPSQI调查，抑郁症现患125例，睡眠障碍（PSQI总分〉7）的发生比率为68．8％；PSQI总分与有无支持群体、社会环境、教育、职业、住房、经济、卫生保健、法律与犯罪等社会心理与环境问题无相关。结论睡眠障碍是抑郁症的常见症状，受社会心理与环境问题的影响较小。     

促肾上腺皮质激素释放激素受体1基因多态与抗抑郁药物疗效的关联研究

目的探讨促肾上腺皮质激素释放激素受体1(corticotropin-releasing hormone receptor1,CRHR1)基因多态性与选择性5-羟色胺再摄取抑制剂(Selective Serotonin Reuptake Inhibitors,SSRIs)、5-羟色胺和去甲肾上腺素再摄取抑制剂(Serotonin and Norepinephrine Reuptake Inhibitors,SNRIs)抗抑郁疗效差异的相关性。方法对符合美国精神障碍诊断与统计手册第4版(Diagnostic and Statistical Manual of Mental Disorders,Fourth Edi-tion,DSM-Ⅳ)抑郁症诊断标准的271例抑郁症患者予以单一新型抗抑郁药(SSRIs或SNRIs)常规剂量治疗至少6周,以治疗前后17项汉密尔顿抑郁量表(Hamilton Depression Scale,HAMD)总分减分率作为评估疗效的指标。采用TaqMan探针法检测CRHR1基因上4个单核苷酸多态性(Single Nucleotide Polymorphism,SNP)的基因型,比较有效组(HAMD-17减分率≥50%)和无效组(HAMD-17减分率<50%)之间4个位点基因型及多位点组成单倍型的不同。结果治疗4周末:CRHR1基因rs17689966位点A等位基因及AA基因型携带者在治疗无效组的频率均显著高于有效组(88.0%vs.77.0%,P=0.004;75.8%vs.59.0%,P=0.004)。有3种单倍型在有效组和无效组之间的分布差异有统计学意义,分别是T-A/T-G(rs242924-rs17689966:86.6%vs.74.7%,P=0.002;8.1%vs.15.5%,P=0.018),G-T-G(rs4458044-rs rs242924-rs17689966:8.2%vs.15.5%,P=0.019)。治疗6周末:CRHR1基因4个SNPs的基因型、等位基因频率及单倍型分析在不同疗效患者组间分布差异均无统计学意义(均P>0.05)。结论CRHR1基因多态性可能与SSRIs、SNRIs类药物的早期疗效相关。     

Predictors of depressive symptoms at hospital discharge in patients with major depressive disorder

Abstract

Objective. Often patients with major depressive disorder (MDD) leave the hospital with continued significant symptomatology. This study sought to evaluate demographic, clinical, and psychosocial predictors of the presence of clinically significant depressive symptoms, defined as a Modified Hamilton Rating Scale for Depression score of ≥ 14, immediately following hospitalization for MDD. Methods. The study enrolled 135 patients with MDD as part of a larger clinical trial investigating the efficacy of post-hospitalization pharmacologic and psychosocial treatments for depressed inpatients. Structured clinical interview and self-report data were available from 126 patients at hospital admission and discharge. Results. Despite the significant decreases in depressive symptoms over the course of hospitalization, 91 (72%) displayed clinically significant depressive symptoms at discharge. Multivariate logistic regression analysis revealed that female sex, earlier age of onset, and poorer social adjustment were unique predictors of symptom outcome. Conclusions. Results suggest that a large proportion of patients leave the hospital with continued significant symptomatology, and the presence of such symptoms following hospitalization for MDD is likely to be explained by a combination of factors.     

具有抗炎作用的药物在抑郁症治疗中的研究进展

抑郁症是常见的精神疾病之一,其发病机制尚未完全明确,机体炎症水平升高是目前公认的抑郁症发病机制之一。大量研究表明,非甾体类抗炎药、ω-3脂肪酸、他汀类药物、吡格列酮、米诺环素、N-乙酰半胱氨酸、皮质类固醇等药物可能通过抗炎作用发挥抗抑郁疗效。本文就上述药物在抗抑郁治疗中的应用进行综述,探讨具有抗炎作用的药物对抑郁症治疗的效果及其可能的作用机制,为未来抗炎干预在抑郁症治疗中的应用提供参考。     

Nuclear receptors modulate inflammasomes in the pathophysiology and treatment of major depressive disorder

Major depressive disorder (MDD) is highly prevalent and is a significant cause of mortality and morbidity worldwide. Currently, conventional pharmacological treatments for MDD produce temporary remission in < 50% of patients; therefore, there is an urgent need for a wider spectrum of novel antidepressants to target newly discovered underlying disease mechanisms. Accumulated evidence has shown that immune inflammation, particularly inflammasome activity, plays an important role in the pathophysiology of MDD. In this review, we summarize the evidence on nuclear receptors (NRs), such as glucocorticoid receptor, mineralocorticoid receptor, estrogen receptor, aryl hydrocarbon receptor, and peroxisome proliferator-activated receptor, in modulating the inflammasome activity and depression-associated behaviors. This review provides evidence from an endocrine perspective to understand the role of activated NRs in the pathophysiology of MDD, and to provide insight for the discovery of antidepressants with novel mechanisms for this devastating disorder.     

首发精神分裂症与双相障碍及抑郁障碍认知功能比较

目的探讨首发精神分裂症、双相障碍及抑郁障碍患者认知功能差异。方法纳入首发精神分裂症患者61例,双相障碍患者57例,抑郁障碍患者48例,另设正常对照59名。所有研究对象采用重复性神经心理测查系统(Repeatable Battery for the Assessment of Neuropsychological Status,RBANS)评估认知功能,首发精神分裂症组采用阳性和阴性症状量表(positive and negative syndrome scale,PANSS)评定精神病性症状,双相障碍组、抑郁障碍组采用汉密尔顿抑郁量表(Hamilton depression scale,HAMD)、汉密尔顿焦虑量表(Hamilton anxiety scale,HAMA)评估抑郁和焦虑症状,贝克—拉范森躁狂(Bech-Rafaelsen mania scale,BRMS)量表评估躁狂症状。结果 4组对象的RBANS总分(F=5.18,P0.01)、即刻记忆(F=4.09,P0.01)、言语功能(F=9.53,P0.01)、注意(F=3.87,P=0.01)、延时记忆(F=9.86,P0.01)因子得分差异具有统计学意义,其中首发精神分裂症、双相障碍组RBANS总分低于对照组(P0.01),首发精神分裂症、双相障碍、抑郁障碍组即刻记忆、言语功能、延时记忆得分低于对照组(P0.05),双相障碍组言语功能得分低于首发精神分裂症组(P0.01),首发精神分裂症组注意得分低于抑郁障碍及对照组(P0.01)。结论首发精神分裂症、双相障碍、抑郁障碍患者均存在认知功能损伤,首发精神分裂症认知功能缺陷重于抑郁障碍,轻于双相障碍。     

抑郁症与精神分裂症患者心率变异性的对照分析

目的探讨抑郁症与精神分裂症患者的心率变异性（HRV）的差异。方法对36例首次发作的抑郁症患者及年龄、性别与之相匹配的41例首次发作的精神分裂症患者分别进行短时程HRV检测,并对其心率变异指标SDNN、MSD、rMSSD、PNN50、LF、HF、LF/HF结果进行分析。结果抑郁症患者的时阈指标rMSSD（P〈0.05）、PNN50（P〈0.01）较精神分裂症显著降低,而两者之间的频阈分析指标无明显差异。结论抑郁症患者的自主神经功能失调较精神分裂症患者更严重。     

阿戈美拉汀治疗重度抑郁症的临床疗效

目的 探讨新型抗抑郁药物阿戈美拉汀在治疗重度抑郁患者方面的临床疗效和安全性.方法 选取我院2013年2月～2014年2月收住院的重度抑郁症患者58例随机分为两组,研究组应用阿戈美拉汀25～50mg/d,平均剂量（46.36±4.48）mg/d,对照组选用艾司西酞普兰10～20mg/d,平均剂量（16.83±2.94）mg/d,均治疗8周.治疗前及治疗后第2,4,8周分别采用汉密尔顿抑郁量表（HAMD-17）对两组进行评估,在治疗过程中应用治疗不良反应量表（TESS）进行测量.结果 治疗2周后研究组HAMD减分为（8.36±4.07）分,对照组为（6.19±3.68）分,两组减分情况比较差异有统计学意义（q=3.38,P＜0.05）.治疗8周后阿戈美拉汀组HAMD减分为（18.15±4.29）分,艾司西酞普兰组HAMD减分为（16.26±3.83）分,两组减分情况比较差异有统计学意义（q=4.12,P＜ 0.05）.药物安全性方面,研究组主要不良反应依次是头痛（5例）、便秘（4例）和肝功能异常（3例）;对照组主要不良反应依次是头痛（9例）、恶心呕吐（6例）和血压升高（5例）.TESS总分比较,研究组（3.42±1.24）分低于对照组（4.08±1.69）分,差异有统计学意义（t=7.45,P＜0.01）.结论 阿戈美拉汀在治疗重度抑郁症方面,较艾司西酞普兰起效快,疗效明显,不良反应少.     

The role of nesfatin-1 in impaired appetite in patients with major depressive disorder

AimThe aim of the present study was to explore whether plasma nesfatin-1 levels are associated with impaired appetite in major depressive disorder (MDD).MethodsPatients were recruited from outpatients who consecutively sought treatment in the psychiatric outpatient clinic of the University Hospital since March 2012. All patients were diagnosed with major depressive disorder according to DSM-IV. The appetite of patients was assessed by specific questionnaire. We categorized patients into two groups according to their appetite. Study group consisted of 30 patients with increased appetite (MDD-IA), 28 patients with decreased appetite (MDD-DA) and 28 healthy controls. Plasma nesfatin-1 levels and body mass index (BMI) were measured.ResultsThere was no statistically significant difference in nesfatin-1 between groups. The mean serum nesfatin-1 level did not show any correlation with age, BMI, HAM-D scores and fasting blood glucose in patients groups.ConclusionOur findings suggest that fasting plasma nesfatin-1 levels are unchanged in untreated MDD patients and there is no evidence for nesfatin-1 playing a role in impaired appetite in patients with MDD.     

重性抑郁障碍患者药物治疗反应相关自发性神经活动改变的Meta分析

目的探索重性抑郁障碍(MDD)患者与药物治疗反应相关的自发性神经活动改变,寻找与治疗反应相关的影像学指标。方法计算机检索中国知网数据库、万方数据库、维普数据库、PubMed、Embase和Web of Science数据库,收集与MDD患者治疗反应相关的静息态脑功能影像研究,使用AES-SDM进行Meta分析。结果共8篇文章纳入Meta分析,包括288例患者和304例健康对照组。Meta分析结果显示,与健康对照组相比,治疗有效的MDD患者左侧小脑(峰值坐标:X=-22,Y=-78,Z=-18,SDM-Z=1.458)、左侧颞叶(峰值坐标:X=-50,Y=-30,Z=-8,SDM-Z=1.539)及右侧角回(峰值坐标:X=48,Y=-66,Z=36,SDM-Z=1.536)的脑功能活动增加,左侧辅助运动区(峰值坐标:X=-10,Y=-2,Z=72,SDM-Z=-1.107)脑功能活动降低;治疗无效的MDD患者双侧额上回、前扣带回(峰值坐标:X=12,Y=42,Z=-4,SDM-Z=1.526)脑功能活动增加,左侧额下回(峰值坐标:X=-48,Y=16,Z=6,SDM-Z=-1.912)脑功能活动降低。结论小脑半球自发性神经活动的改变可能成为预测MDD患者治疗反应的影像学指标。     

Pharmacogenomic predictors of citalopram treatment outcome in major depressive disorder

Objectives. A significant proportion of patients with major depressive disorder (MDD) do not improve following treatment with first-line antidepressants and, currently, there are no objective indicators of predictors of antidepressant response. The aim of this study was to investigate pre-treatment peripheral gene expression differences between future remitters and non-responders to citalopram treatment and identify potential pharmacogenomic predictors of response. Methods. We conducted a gene expression study using Affymetrix HG-U133 Plus2 microarrays in peripheral blood samples from untreated individuals with MDD (N = 77), ascertained at a community outpatient clinic, prior to an 8-week treatment with citalopram. Gene expression differences were assessed between remitters and non-responders to treatment. Technical validation of significant probesets was carried out by qRT-PCR. Results. A total of 434 probesets displayed significant correlation to change in score and 33 probesests were differentially expressed between eventual remitters and non-responders. Probesets for SMAD 7 (SMA- and MAD-related protein 7) and SIGLECP3 (sialic acid-binding immunoglobulin-like lectin, pseudogene 3) were the most significant differentially expressed genes following FDR correction, and both were down-regulated in individuals who responded to treatment. Conclusions. These findings point to SMAD7 and SIGLECP3 as candidate predictive biomarkers of antidepressant response.