Previous studies on reporting bias generally examined whether trials were published in stand-alone publications. In this study, we investigated whether pooled-trials publications constitute a specific form of reporting bias. We assessed whether negative trials were more likely to be exclusively published in pooled-trials publications than positive trials and examined the research questions, individual trial results, and conclusions presented in these articles.

Data from a cohort of 105 randomized controlled trials of 16 antidepressants were extracted from earlier publications and the corresponding Food and Drug Administration (FDA) reviews. A systematic literature search was conducted to identify pooled-trials publications.

We found 107 pooled-trials publications that reported results of 23 (72%) of 32 trials not published in stand-alone publications. Only two (3.8%) of 54 positive trials were published exclusively in pooled-trials publications, compared with 21 (41.1%) of 51 negative trials (p < 0.001). Thirteen (12%) of 107 publications had as primary aim to present data on the trial's primary research question (drug efficacy compared with placebo). Only four of these publications, reporting on five (22%) trials, presented individual efficacy data for the primary research question. Additionally, only five (5%) of 107 pooled-trials publications had a negative conclusion.

Compared with positive trials, negative trials of antidepressants for depression were much more likely to be reported exclusively in pooled-trials publications. Pooled-trials publications flood the evidence base with often-redundant articles that, instead of addressing the original primary research question, present (positive) results on secondary questions. Therefore, pooled-trials publications distort the apparent risk–benefit profile of antidepressants.

Converging lines of evidence implicate an important role for the immune system in schizophrenia. Microglia are the resident immune cells of the central nervous system and have many functions including neuroinflammation, axonal guidance and neurotrophic support. We aimed to provide a quantitative review of in vivo PET imaging studies of microglia activation in patients with schizophrenia compared with healthy controls.

Demographic, clinical and imaging measures were extracted from each study and meta-analysis was conducted using a random-effects model (Hedge's g). The difference in 18-kDa translocator protein (TSPO) binding between patients with schizophrenia and healthy controls, as quantified by either binding potential (BP) or volume of distribution (VT), was used as the main outcome. Sub-analysis and sensitivity analysis were carried out to investigate the effects of genotype, ligand and illness stage.

In total, 12 studies comprising 190 patients with schizophrenia and 200 healthy controls met inclusion criteria. There was a significant elevation in tracer binding in schizophrenia patients relative to controls when BP was used as an outcome measure, (Hedge's g = 0.31; p = 0.03) but no significant differences when VT was used (Hedge's g = −0.22; p = 0.29).

In conclusion, there is evidence for moderate elevations in TSPO tracer binding in grey matter relative to other brain tissue in schizophrenia when using BP as an outcome measure, but no difference when VT is the outcome measure. We discuss the relevance of these findings as well as the methodological issues that may underlie the contrasting difference between these outcomes.

Self-harm in young people is associated with later problems in social and emotional development. However, it is unknown whether self-harm in young women continues to be a marker of vulnerability on becoming a parent. This study prospectively describes the associations between pre-conception self-harm, maternal depressive symptoms and mother–infant bonding problems.

The Victorian Intergenerational Health Cohort Study (VIHCS) is a follow-up to the Victorian Adolescent Health Cohort Study (VAHCS) in Australia. Socio-demographic and health variables were assessed at 10 time-points (waves) from ages 14 to 35, including self-reported self-harm at waves 3–9. VIHCS enrolment began in 2006 (when participants were aged 28–29 years), by contacting VAHCS women every 6 months to identify pregnancies over a 7-year period. Perinatal depressive symptoms were assessed with the Edinburgh Postnatal Depression Scale during the third trimester, and 2 and 12 months postpartum. Mother–infant bonding problems were assessed with the Postpartum Bonding Questionnaire at 2 and 12 months postpartum.

Five hundred sixty-four pregnancies from 384 women were included. One in 10 women (9.7%) reported pre-conception self-harm. Women who reported self-harming in young adulthood (ages 20–29) reported higher levels of perinatal depressive symptoms and mother–infant bonding problems at all perinatal time points [perinatal depressive symptoms adjusted β = 5.40, 95% confidence interval (CI) 3.42–7.39; mother–infant bonding problems adjusted β = 7.51, 95% CI 3.09–11.92]. There was no evidence that self-harm in adolescence (ages 15–17) was associated with either perinatal outcome.

Self-harm during young adulthood may be an indicator of future vulnerability to perinatal mental health and mother–infant bonding problems.

Individuals with autism spectrum disorder (ASD) appear to be at increased risk of non-affective psychotic disorder (NAPD) and bipolar disorder (BD). However, most previous studies examined the co-occurrence of ASD and NAPD or BD, ignoring possible diagnostic bias and selection bias. We used longitudinal data from Dutch psychiatric case registers to assess the risk of NAPD or BD among individuals with ASD, and compared the results to those obtained for the Dutch population in earlier studies.

Individuals with ASD (n = 17 234) were followed up between 16 and 35 years of age. Kaplan–Meier estimates were used to calculate the risk of NAPD or BD. We conducted separate analyses to reduce possible bias, including an analysis among individuals diagnosed with ASD before age 16 years (n = 8337).

Of the individuals with ASD, 23.50% (95% confidence interval 21.87–25.22) were diagnosed with NAPD and 3.79% (3.06–4.69) with BD before age 35 years. The corresponding figures for the general population were 0.91% (0.63–1.28) and 0.13% (0.08–0.20). Risk estimates were substantially lower, but still higher than general population estimates, when we restricted our analyses to individuals diagnosed with ASD before age 16, with 1.87% (1.33–2.61) being diagnosed with NAPD and 0.57% (0.21–1.53) with BD before age 25 years. The corresponding figures for the general population were 0.63% (0.44–0.86) and 0.08% (0.05–0.12).

Individuals with ASD are at increased risk of NAPD or BD. This is likely not the result of diagnostic or selection bias.

Abnormalities in reward circuit function are considered a core feature of addiction. Yet, it is still largely unknown whether these abnormalities stem from chronic drug use, a genetic predisposition, or both.

In the present study, we investigated this issue using a large sample of adolescent children by applying structural equation modeling to examine the effects of several dopaminergic polymorphisms of the D1 and D2 receptor type on the reward function of the ventral striatum (VS) and orbital frontal cortex (OFC), and whether this relationship predicted the propensity to engage in early alcohol misuse behaviors at 14 years of age and again at 16 years of age.

The results demonstrated a regional specificity with which the functional polymorphism rs686 of the D1 dopamine receptor (DRD1) gene and Taq1A of the ANKK1 gene influenced medial and lateral OFC activation during reward anticipation, respectively. Importantly, our path model revealed a significant indirect relationship between the rs686 of the DRD1 gene and early onset of alcohol misuse through a medial OFC × VS interaction.

These findings highlight the role of D1 and D2 in adjusting reward-related activations within the mesocorticolimbic circuitry, as well as in the susceptibility to early onset of alcohol misuse.

Conveying information cohesively is an essential element of communication that is disrupted in schizophrenia. These disruptions are typically expressed through disorganized symptoms, which have been linked to neurocognitive, social cognitive, and metacognitive deficits. Automated analysis can objectively assess disorganization within sentences, between sentences, and across paragraphs by comparing explicit communication to a large text corpus.

Little work in schizophrenia has tested: (1) links between disorganized symptoms measured via automated analysis and neurocognition, social cognition, or metacognition; and (2) if automated analysis explains incremental variance in cognitive processes beyond clinician-rated scales. Disorganization was measured in schizophrenia (n = 81) with Coh-Metrix 3.0, an automated program that calculates basic and complex language indices. Trained staff also assessed neurocognition, social cognition, metacognition, and clinician-rated disorganization.

Findings showed that all three cognitive processes were significantly associated with at least one automated index of disorganization. When automated analysis was compared with a clinician-rated scale, it accounted for significant variance in neurocognition and metacognition beyond the clinician-rated measure. When combined, these two methods explained 28–31% of the variance in neurocognition, social cognition, and metacognition.

This study illustrated how automated analysis can highlight the specific role of disorganization in neurocognition, social cognition, and metacognition. Generally, those with poor cognition also displayed more disorganization in their speech—making it difficult for listeners to process essential information needed to tie the speaker's ideas together. Our findings showcase how implementing a mixed-methods approach in schizophrenia can explain substantial variance in cognitive processes.

Assertive Community Treatment (ACT) is an evidence-based treatment program for people with severe mental illness developed in high-income countries. We report the first randomized controlled trial of ACT in mainland China.

Sixty outpatients with schizophrenia with severe functional impairments or frequent hospitalizations were randomly assigned to ACT (n = 30) or standard community treatment (n = 30). The severity of symptoms and level of social functioning were assessed at baseline and every 3 months during the 1-year study. The primary outcome was the duration of hospital readmission. Secondary outcomes included a pre-post change in symptom severity, the rates of symptom relapse and gainful employment, social and occupational functioning, and quality of life of family caregivers.

Based on a modified intention-to-treat analysis, the outcomes for ACT were significantly better than those of standard community treatment. ACT patients were less likely to be readmitted [3.3% (1/30) v. 25.0% (7/28), Fisher's exact test p = 0.023], had a shorter mean readmission time [2.4 (13.3) v. 30.7 (66.9) days], were less likely to relapse [6.7% (2/30) v. 28.6% (8/28), Fisher's exact test p = 0.038], and had shorter mean time in relapse [3.5 (14.6) v. 34.4 (70.6) days]. The ACT group also had significantly longer times re-employed and greater symptomatic improvement and their caregivers experienced a greater improvement in their quality of life.

Our results show that culturally adapted ACT is both feasible and effective for individuals with severe schizophrenia in urban China. Replication studies with larger samples and longer duration of follow up are warranted.

Much of the interest in youth at clinical high risk (CHR) of psychosis has been in understanding conversion. Recent literature has suggested that less than 25% of those who meet established criteria for being at CHR of psychosis go on to develop a psychotic illness. However, little is known about the outcome of those who do not make the transition to psychosis. The aim of this paper was to examine clinical symptoms and functioning in the second North American Prodrome Longitudinal Study (NAPLS 2) of those individuals whose by the end of 2 years in the study had not developed psychosis.

In NAPLS-2 278 CHR participants completed 2-year follow-ups and had not made the transition to psychosis. At 2-years the sample was divided into three groups – those whose symptoms were in remission, those who were still symptomatic and those whose symptoms had become more severe.

There was no difference between those who remitted early in the study compared with those who remitted at one or 2 years. At 2-years, those in remission had fewer symptoms and improved functioning compared with the two symptomatic groups. However, all three groups had poorer social functioning and cognition than healthy controls.

A detailed examination of the clinical and functional outcomes of those who did not make the transition to psychosis did not contribute to predicting who may make the transition or who may have an earlier remission of attenuated psychotic symptoms.

Elevated levels of pro-inflammatory cytokines are consistently reported in schizophrenia (SZ) and bipolar-I disorder (BD), as well as among individuals who have been exposed to childhood trauma. However, higher levels of inflammatory markers in these disorders are yet to be investigated with respect to levels of exposure to different types of childhood trauma.

Participants were 68 cases with a diagnosis of schizophrenia/schizoaffective disorder (SZ), 69 cases with a diagnosis of psychotic BD and 72 healthy controls (HC). Serum levels of interleukin 6 (IL-6), tumour necrosis factor-α (TNF-α) and C-reactive protein (CRP) were quantified, and childhood trauma exposure was assessed with the Childhood Trauma Questionnaire.

The SZ group had significantly higher levels of IL-6, TNF-α and CRP when compared with the HC group (all p < 0.05, d = 0.41–0.63), as well as higher levels of TNF-α when compared with the BD group (p = 0.014, d = 0.50); there were no differences between the BD and HC groups for any markers. Exposure to sexual abuse was positively associated (standardised β = 0.326, t = 2.459, p = 0.018) with levels of CRP in the SZ group, but there were no significant associations between any form of trauma exposure and cytokine levels in the HC or BD groups.

These results contribute to the evidence for a chronic state of inflammation in SZ but not BD cases. Differential associations between trauma exposure and levels of pro-inflammatory cytokines across the diagnostic categories suggest that trauma may impact biological (stress and immune) systems differently in these patient groups.

Despite the well-documented association between smoking and personality traits such as neuroticism and extraversion, little is known about the potential causal nature of these findings. If it were possible to unpick the association between personality and smoking, it may be possible to develop tailored smoking interventions that could lead to both improved uptake and efficacy.

Recent genome-wide association studies (GWAS) have identified variants robustly associated with both smoking phenotypes and personality traits. Here we use publicly available GWAS summary statistics in addition to individual-level data from UK Biobank to investigate the link between smoking and personality. We first estimate genetic overlap between traits using LD score regression and then use bidirectional Mendelian randomisation methods to unpick the nature of this relationship.

We found clear evidence of a modest genetic correlation between smoking behaviours and both neuroticism and extraversion. We found some evidence that personality traits are causally linked to certain smoking phenotypes: among current smokers each additional neuroticism risk allele was associated with smoking an additional 0.07 cigarettes per day (95% CI 0.02–0.12, p = 0.009), and each additional extraversion effect allele was associated with an elevated odds of smoking initiation (OR 1.015, 95% CI 1.01–1.02, p = 9.6 × 10−7).

We found some evidence for specific causal pathways from personality to smoking phenotypes, and weaker evidence of an association from smoking initiation to personality. These findings could be used to inform future smoking interventions or to tailor existing schemes.

Etiological research of depression and anxiety disorders has been hampered by diagnostic heterogeneity. In order to address this, researchers have tried to identify more homogeneous patient subgroups. This work has predominantly focused on explaining interpersonal heterogeneity based on clinical features (i.e. symptom profiles). However, to explain interpersonal variations in underlying pathophysiological mechanisms, it might be more effective to take biological heterogeneity as the point of departure when trying to identify subgroups. Therefore, this study aimed to identify data-driven subgroups of patients based on biomarker profiles.

Data of patients with a current depressive and/or anxiety disorder came from the Netherlands Study of Depression and Anxiety, a large, multi-site naturalistic cohort study (n = 1460). Thirty-six biomarkers (e.g. leptin, brain-derived neurotrophic factor, tryptophan) were measured, as well as sociodemographic and clinical characteristics. Latent class analysis of the discretized (lower 10%, middle, upper 10%) biomarkers were used to identify different patient clusters.

The analyses resulted in three classes, which were primarily characterized by different levels of metabolic health: ‘lean’ (21.6%), ‘average’ (62.2%) and ‘overweight’ (16.2%). Inspection of the classes’ clinical features showed the highest levels of psychopathology, severity and medication use in the overweight class.

The identified classes were strongly tied to general (metabolic) health, and did not reflect any natural cutoffs along the lines of the traditional diagnostic classifications. Our analyses suggested that especially poor metabolic health could be seen as a distal marker for depression and anxiety, suggesting a relationship between the ‘overweight’ subtype and internalizing psychopathology.

An increasing importance is being placed on mental health and wellbeing at individual and population levels. While there are several interventions that have been proposed to improve wellbeing, more evidence is needed to understand which aspects of wellbeing are most influential. This study aimed to identify key items that signal improvement of mental health and wellbeing.

Using network analysis, we identified the most central items in the graph network estimated from the well-established Warwick-Edinburgh Mental Well-being Scale (WEMWBS). Results were compared across four major UK cohorts comprising a total of 47,578 individuals: the Neuroscience in Psychiatry Network, the Scottish Schools Adolescent Lifestyle and Substance Use Survey, the Northern Ireland Health Survey, and the National Child Development Study.

Regardless of gender, the three items most central in the network were related to positive self-perception and mood: ‘I have been feeling good about myself’; ‘I have been feeling confident’; and ‘I have been feeling cheerful’. Results were consistent across all four cohorts.

Positive self-perception and positive mood are central to psychological wellbeing. Psychotherapeutic and public mental health interventions might best promote psychological wellbeing by prioritising the improvement of self-esteem, self-confidence and cheerfulness. However, empirical testing of interventions using these key targets is needed.

Polycystic ovary syndrome (PCOS) is associated with increased psychological distress in clinical populations. We aimed to assess depression, anxiety and perceived stress in women with and without PCOS in a large community-based sample and investigate the role of stress in contributing to and mediating the relationship between PCOS, depression and anxiety.

A cross-sectional analysis was performed from the Australian Longitudinal Study of Women's Health (ALWSH) comparing women with (n = 478) or without (n = 8134) a self-reported diagnosis of PCOS. Main outcome measures were depression, anxiety and perceived stress measured using validated scales. The χ2 and t tests were used to assess differences between groups. Univariable and multivariable regression were performed to determine factors contributing to each outcome.

Women reporting PCOS, compared with women not reporting PCOS, reported higher prevalence of depression (27.3% v. 18.8%), anxiety symptoms (50% v. 39.2%) and greater score for perceived stress (1.01 ± 0.03 v. 0.88 ± 0.01). After adjusting for body mass index, infertility and socio-demographic factors, women with PCOS were still more likely to be depressed, anxious and to have a higher level of perceived stress. There was a high-level mediation effect of stress between PCOS and both depression and anxiety.

Compared with women not reporting PCOS, women reporting PCOS have increased depression, anxiety and perceived stress. Stress may play a role in the association between PCOS, depression and anxiety. Further studies should consider assessment and management of stress in PCOS as it may be relevant for understanding the aetiology and treatment of psychological distress.

Emerging adulthood is a peak period of risk for alcohol and illicit drug use. Recent advances in psychiatric genetics suggest that the co-occurrence of substance use and psychopathology arises, in part, from a shared genetic etiology. We sought to extend this research by investigating the influence of genetic risk for schizophrenia on trajectories of four substance use behaviors as they occurred across emerging adulthood.

Young adult participants of non-Hispanic European descent provided DNA samples and completed daily reports of substance use for 1 month per year across 4 years (N = 30 085 observations of N = 342 participants). A schizophrenia polygenic score was included in two-level hierarchical linear models designed to test associations between genetic risk for schizophrenia, participant age, and four substance use phenotypes.

Participants with a greater schizophrenia polygenic score experienced greater age-related increases in the likelihood of using substances across emerging adulthood (p < 0.005). Additionally, our results suggest that the polygenic score was positively associated with participants’ overall likelihood to engage in illicit drug use but not alcohol-related substance use.

This study used a novel combination of polygenic prediction and intensive longitudinal methods to characterize the influence of genetic risk for schizophrenia on patterns of age-related change in substance use across emerging adulthood. Results suggest that genetic risk for schizophrenia has developmentally specific effects on substance use behaviors in a non-clinical population of young adults.

Abnormal thyroid function is prevalent among women and has been linked to increased risk of chronic disease. Posttraumatic stress disorder (PTSD) has been linked to thyroid dysfunction in some studies; however, the results have been inconsistent. Thus, we evaluated trauma exposure and PTSD symptoms in relation to incident thyroid dysfunction in a large longitudinal cohort of civilian women.

We used data from 45 992 women from the ongoing Nurses’ Health Study II, a longitudinal US cohort study that began in 1989. In 2008, history of trauma and PTSD were assessed with the Short Screening Scale for Diagnostic and Statistical Manual of Mental Disorders, fourth edition, PTSD, and incident thyroid dysfunction was determined by participants’ self-report in biennial questionnaires of physician-diagnosed hypothyroidism and Graves’ hyperthyroidism. The study period was from 1989 to 2013. Proportional hazard models were used to estimate multivariable-adjusted hazard ratios and 95% confidence intervals (CIs) for incident hypothyroidism and Graves’ hyperthyroidism.

In multivariable-adjusted models, we found significant associations for PTSD only with hypothyroidism [p-trend <0.001; trauma with no PTSD symptoms, 1.08 (95% CI 1.02–1.15); 1–3 PTSD symptoms, 1.12 (95% CI 1.04–1.21); 4–5 PTSD symptoms, 1.23 (95% CI 1.13–1.34); and 6–7 PTSD symptoms, 1.26 (95% CI 1.14–1.40)]. PTSD was not associated with risk of Graves’ hyperthyroidism (p-trend = 0.34). Associations were similar in sensitivity analyses restricted to outcomes with onset after 2008, when PTSD was assessed.

PTSD was associated with higher risk of hypothyroidism in a dose-dependent fashion. Highlighted awareness for thyroid dysfunction may be especially important in women with PTSD.

Studies have consistently shown that subthreshold depression is associated with an increased risk of developing major depression. However, no study has yet calculated a pooled estimate that quantifies the magnitude of this risk across multiple studies.

We conducted a systematic review to identify longitudinal cohort studies containing data on the association between subthreshold depression and future major depression. A baseline meta-analysis was conducted using the inverse variance heterogeneity method to calculate the incidence rate ratio (IRR) of major depression among people with subthreshold depression relative to non-depressed controls. Subgroup analyses were conducted to investigate whether IRR estimates differed between studies categorised by age group or sample type. Sensitivity analyses were also conducted to test the robustness of baseline results to several sources of study heterogeneity, such as the case definition for subthreshold depression.

Data from 16 studies (n = 67 318) revealed that people with subthreshold depression had an increased risk of developing major depression (IRR = 1.95, 95% confidence interval 1.28–2.97). Subgroup analyses estimated similar IRRs for different age groups (youth, adults and the elderly) and sample types (community-based and primary care). Sensitivity analyses demonstrated that baseline results were robust to different sources of study heterogeneity.

The results of this study support the scaling up of effective indicated prevention interventions for people with subthreshold depression, regardless of age group or setting.

Existing evidence for gene × environment interaction (G × E) in neuroticism largely relies on candidate gene studies, although neuroticism is highly polygenic. This study aimed to investigate the long-term associations between polygenic risk scores for neuroticism (PRSN), objective childhood adversity and their interplay on emotional health aspects such as neuroticism itself, depressive symptoms, anxiety symptoms, loneliness and life satisfaction.

The sample consisted of reared-apart (TRA) and reared-together (TRT) middle- and old age twins (N = 699; median age at separation = 2). PRSN were created under nine p value cut-off thresholds (pT-s) and the pT with the highest degree of neuroticism variance explained was chosen for subsequent analyses. Linear regressions were used to assess the associations between PRSN, childhood adversity (being reared apart) and emotional health. G × E was further investigated using a discordant twin design.

PRSN explained up to 1.7% (pT < 0.01) of phenotypic neuroticism in the total sample. Analyses across two separation groups revealed substantial heterogeneity in the variance explained by PRSN; 4.3% was explained in TRT, but almost no effect was observed in TRA. Similarly, PRSN explained 4% and 1.7% of the variance in depressive symptoms and loneliness, respectively, only in TRT. A significant G × E interaction was identified for depressive symptoms.

By taking advantage of a unique sample of adopted twins, we demonstrated the presence of G × E in neuroticism and emotional health using PRSN and childhood adversity. Our results may indicate that genome-wide association studies are detecting genetic main effects associated with neuroticism, but not those susceptible to early environmental influences.

There is evidence for the cost-effectiveness of health visitor (HV) training to assess postnatal depression (PND) and deliver psychological approaches to women at risk of depression. Whether this approach is cost-effective for lower-risk women is unknown. There is a need to know the cost of HV-delivered universal provision, and how much it might cost to improve health-related quality of life for postnatal women. A sub-study of a cluster-randomised controlled trial in the former Trent region (England) previously investigated the effectiveness of PoNDER HV training in mothers at lower risk of PND. We conducted a parallel cost-effectiveness analysis at 6-months postnatal for all mothers with lower-risk status attributed to an Edinburgh Postnatal Depression Scale (EPDS) score <12 at 6-weeks postnatal.

Intervention HVs were trained in assessment and cognitive behavioural or person-centred psychological support techniques to prevent depression. Outcomes examined: quality-adjusted life-year (QALY) gains over the period between 6 weeks and 6 months derived from SF-6D (from SF-36); risk-of-depression at 6 months (dichotomising 6-month EPDS scores into lower risk (<12) and at-risk (⩾12).

In lower-risk women, 1474 intervention (63 clusters) and 767 control participants (37 clusters) had valid 6-week and 6-month EPDS scores. Costs and outcomes data were available for 1459 participants. 6-month adjusted costs were £82 lower in intervention than control groups, with 0.002 additional QALY gained. The probability of cost-effectiveness at £20 000 was very high (99%).

PoNDER HV training was highly cost-effective in preventing symptoms of PND in a population of lower-risk women and cost-reducing over 6 months.

The transcriptional coactivator peroxisome proliferator-activated receptor-γ coactivator (PGC-1α), termed the ‘master regulator of mitochondrial biogenesis’, has been implicated in stress and resilience to stress-induced depressive-like behaviours in animal models. However, there has been no study conducted to date to examine PGC-1α levels in patients with depression or in response to antidepressant treatment. Our aim was to assess PGC-1α mRNA levels in blood from healthy controls and patients with depression pre-/post-electroconvulsive therapy (ECT), and to examine the relationship between blood PGC-1α mRNA levels and clinical symptoms and outcomes with ECT.

Whole blood PGC-1α mRNA levels were analysed in samples from 67 patients with a major depressive episode and 70 healthy controls, and in patient samples following a course of ECT using quantitative real-time polymerase chain reaction (qRT-PCR). Exploratory subgroup correlational analyses were carried out to determine the relationship between PGC-1α and mood scores.

PGC-1α levels were lower in patients with depression compared with healthy controls (p = 0.03). This lower level was predominantly accounted for by patients with psychotic unipolar depression (p = 0.004). ECT did not alter PGC-1α levels in the depressed group as a whole, though exploratory analyses revealed a significant increase in PGC-1α in patients with psychotic unipolar depression post-ECT (p = 0.045). We found no relationship between PGC-1α mRNA levels and depression severity or the clinical response to ECT.

PGC-1α may represent a novel therapeutic target for the treatment of depression, and be a common link between various pathophysiological processes implicated in depression.

The role of the cerebellum in obsessive-compulsive disorder (OCD) has drawn increasing attention. However, the functional connectivity between the cerebellum and the cerebral cortex has not been investigated in OCD, nor has the relationship between such functional connectivity and clinical symptoms.

A total of 27 patients with OCD and 21 healthy controls (HCs) matched on age, sex and education underwent magnetic resonance imaging (MRI). Seed-based connectivity analyses were performed to examine differences in cerebellar-cerebral connectivity in patients with OCD compared with HCs. Associations between functional connectivity and clinical features in OCD were analyzed.

Compared with HCs, OCD patients showed significantly decreased cerebellar-cerebral functional connectivity in executive control and emotion processing networks. Within the OCD group, decreased functional connectivity in an executive network spanning the right cerebellar Crus I and the inferior parietal lobule was positively correlated with symptom severity, and decreased connectivity in an emotion processing network spanning the left cerebellar lobule VI and the lingual gyrus was negatively correlated with illness duration.

Altered functional connectivity between the cerebellum and cerebral networks involved in cognitive-affective processing in patients with OCD provides further evidence for the involvement of the cerebellum in the pathophysiology of OCD, and is consistent with impairment in executive control and emotion regulation in this condition.