Interleukin-15 is a cytokine that induces or enhances differentiation, maintenance, or activation of several T-cell subsets (including NK, NKT, Th17, Treg, and CD8+ memory cells) and also plays an important role in regulating visceral (intra-abdominal or interstitial) fat breakdown and myofibrillar protein synthesis (hypertrophy). It is also involved in modulating serotonergic activity in the brain by modulating the transmission of GABA and serotonin, which may be the basis for mood and memory disorders, as well as activity levels, sleep, and thermoregulation. Both anorexia nervosa (AN) and schizophrenia (SCH) represent two distinct and serious psychiatric disorders in which some of these symptoms may overlap and where neuroinflammation plays an important role which is yet to be precisely determined.

This article summarizes recent findings and highlights interleukin-15 as a possible link between anorexia nervosa and schizophrenia.

A review of the current literature in the field of psychoneuroimmunology.

In recent years, research has shown elevated levels of IL -15 in the serum of patients suffering from anorexia nervosa and schizophrenia.It is also interesting to note that IL -15 has structural similarities to IL -2, which previous studies have also shown to be elevated in patients with schizophrenia.

These associations, so far suggesting an important role of inflammation and its mediators, need further investigation in light of possible genetic overlap between anorexia nervosa and schizophrenia identified in genome-wide association studies (GWAS).

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Measuring carbon monoxide (CO) in exhaled breath with a visual representation can aid in smoking cessation by increasing smokers’ awareness of how smoking negatively affects their health and how many harmful substances they introduce into their bodies. Individuals attempting to quit smoking can regularly measure CO levels to monitor their progress in reducing this gas in their system.

The national „Smoke Out Day” is a day aimed at encouraging smokers to quit smoking in the Republic of Croatia. It is celebrated on the first day of Lent, as it is a period when most people contemplate giving up something they enjoy throughout the year.

The Institute of Public Health of Virovitičko-podravska County sets up a booth in one of the cities in County on that day. There we offer pamphlets to passersby with information about the harmful effects of smoking and provide them with the opportunity to measure carbon monoxide in their exhaled breath.

The aim of this study was to explore relationship between smoking status, smoke exposure and the levels of exhaled carbon monoxide.

For measuring CO we used piCO simple Smokerlyzer. From April 2015 till May 2023, 462 individuals have participated in this measurement. The data were processed using the Python programming language version 3.9 and the statistical library Pingouin version 0.5.3. Data visualization was performed using the Seaborn library version 0.12.2. The statistical analyses employed in this study are partial correlations. The Spearman method was used for partial correlations because it can identify nonlinear relationships and is more accurate and robust when the assumptions for Pearson correlation are not met.

Partial correlation analysis indicates that there is a statistically significant relationship between the level of carbon monoxide and the following parameters:

• - Non-smoking status in years (rho = -0.526, p <0.001, two-tailed test).

• - Number of cigarettes smoked per day (rho = 0.369, p <0.001, two-tailed test).

• - Testing time after 3 PM (rho = 0.234, p <0.001, two-tailed test).

• - Number of years as a smoker (rho = 0.230, p <0.001, two-tailed test).

• - Age in years (rho = -0.179, p <0.001, two-tailed test).

• - Time spent in a smoky area (rho = 0.114, p <0.016, two-tailed test).

In summary, these results provide valuable insights into the factors associated with carbon monoxide levels in humans, with smoking-related variables, age, and testing time showing notable partial correlations. It is important to consider these relationships when assessing and managing carbon monoxide exposure and its potential health implications.

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Depression and coronary artery disease (CAD) are often comorbid conditions. The presence of depression significantly interferes with the recovery after CAD therapy intervention, such as percutaneous coronary intervention (PCI), one of the most common medical procedures in developed countries. Brain derived neurotrophic factor (BDNF) has a major role in angiogenesis and neuromodulation. Its levels were previously shown to be reduced in patients with depression, and latest studies indicate similar in patients with CAD. However, the correlation of BDNF levels and depression after CAD treatment is unknown.

The aim of this preliminary study is to assess the changes in BDNF levels in patients with depressive symptoms during a six-month period upon PCI.

Antidepressant-free participants that underwent PCI with stent placement due to myocardial infarction or angina pectoris were enrolled in the study. Depressive symptoms were evaluated at baseline using the Beck’s Depression Inventory II (BDI-II) with a cut-off score ≥20 indicating moderate depression. Serum BDNF levels were measured from blood samples drawn a day after (baseline) and six-months upon a successful PCI without complications. The t-test for dependent samples was used with marked significant differences at p<0,05.

Altogether, 76 participants were included in the study, of which 25 finished a six-month follow-up. Participants with BDI-II≥20 at baseline had higher serum BDNF levels in the second measurement (M=23,12, SD=6,20; M=32,02, SD=12,26, respectively). No significant difference was found in serum BDNF levels in measurements between participants with and without depressive symptoms (t=0,33, p=0,74; t=-1,40, p=0,18, respectively). Statistically significant difference was found between serum BDNF in the first and second measurement in the overall sample (t=-2,28, p=0,03) and in participants with baseline moderate depressive symptoms (t=-2,46, p= 0,03), but not in those without (t=-0,59, p=0,57).

Serum BDNF levels in participants with baseline moderate depressive symptoms increased after a six-month period upon successful PCI treatment, whereas that trend was not observed in participants without depressive symptoms. This highlights the potential synergistic role of BDNF in comorbid depression and CAD.

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Depressive symptoms are common in individuals with tinnitus, however, the mechanisms of their interaction are not fully understood. There is neurobiological evidence that might help understanding the interplay between tinnitus and depression which, in turn, helps in making the right choice for treating both conditions.

This case report describes a 70-year old female patient that presented with tinnitus and depressive symptoms lasting for the past 5 years.

The patient showed limited treatment results with different antidepressants. The otorhinolaryngologist ruled out any possible somatic causes of her tinnitus. Tinnitus was causing her sleep disturbances, which worsened her everyday functioning that was already quite poor even further.

After being administered with 30 rounds of TMS, her symptoms either completely resolved or at least reached a level that was adequate for her to start functioning normally on a day-to-day basis.

TMS is a technique that provides non-invasive cortical stimulation, more specifically, when used for depression treatment it stimulates the left dorsolateral prefrontal cortex, a brain region synaptically connected to the limbic system involved in mood regulation that is proven to be hypoactive in depression. The limbic system is where tinnitus-related brain networks and regions involved in the pathophysiology of depression overlap. Further research is needed to deepen the understanding of this topic.

No significant relationships.

No significant relationships.

There is no clinical difference between depressive episodes in bipolar disorder compared to major depressive disorder, which is why bipolar disorder remains unrecognized. Correctly distinguishing these disorders is of great importance because the therapeutic approach differs significantly. According to previous research, zinc, albumin, C reactive protein (CRP), and interleukin-6(IL-6) seem to play a role in differentiating these two types of depressive episodes.

To determine zinc, albumin, CRP and IL-6 serum concentrations in patients with major depressive disorder and depressive episode of bipolar disorder.

Research involved 60 participants. Participants signed informed consent prior to inclusion in the study. Sociodemographic data have been collected using a previously structured questionnaire. The severity of depressive symptoms has been measured by the Montgomery Asberg Depression Rating Scale (MADRS) and the Hamilton Depression Scale (HAM-D-17). Blood samples were obtained from each study participant’s brachial vein, to determine zinc, albumin, C reactive protein and interleukin-6 serum concentrations.

Statistically significant difference was found in zinc serum levels between the two analysed groups. In the overall sample, there is a significant positive correlation between the results on the rating scales and the serum level of CRP.

We confirmed an association between serum levels of CRP and the severity of the illness. Regardless, these are preliminary results of the research. Sufficient final conclusion cannot yet be drawn because it is being limited by the sample size and further investigation is needed.

A cumulative environmental exposure score for schizophrenia (exposome score for schizophrenia [ES-SCZ]) may provide potential utility for risk stratification and outcome prediction. Here, we investigated whether ES-SCZ was associated with functioning in patients with schizophrenia spectrum disorder, unaffected siblings, and healthy controls.

This cross-sectional sample consisted of 1,261 patients, 1,282 unaffected siblings, and 1,525 healthy controls. The Global Assessment of Functioning (GAF) scale was used to assess functioning. ES-SCZ was calculated based on our previously validated method. The association between ES-SCZ and the GAF dimensions (symptom and disability) was analyzed by applying regression models in each group (patients, siblings, and controls). Additional models included polygenic risk score for schizophrenia (PRS-SCZ) as a covariate.

ES-SCZ was associated with the GAF dimensions in patients (symptom: B = −1.53, p-value = 0.001; disability: B = −1.44, p-value = 0.001), siblings (symptom: B = −3.07, p-value < 0.001; disability: B = −2.52, p-value < 0.001), and healthy controls (symptom: B = −1.50, p-value < 0.001; disability: B = −1.31, p-value < 0.001). The results remained the same after adjusting for PRS-SCZ. The degree of associations of ES-SCZ with both symptom and disability dimensions were higher in unaffected siblings than in patients and controls. By analyzing an independent dataset (the Genetic Risk and Outcome of Psychosis study), we replicated the results observed in the patient group.

Our findings suggest that ES-SCZ shows promise for enhancing risk prediction and stratification in research practice. From a clinical perspective, ES-SCZ may aid in efforts of clinical characterization, operationalizing transdiagnostic clinical staging models, and personalizing clinical management.

Psychosis spectrum disorder has a complex pathoetiology characterised by interacting environmental and genetic vulnerabilities. The present study aims to investigate the role of gene–environment interaction using aggregate scores of genetic (polygenic risk score for schizophrenia (PRS-SCZ)) and environment liability for schizophrenia (exposome score for schizophrenia (ES-SCZ)) across the psychosis continuum.

The sample consisted of 1699 patients, 1753 unaffected siblings, and 1542 healthy comparison participants. The Structured Interview for Schizotypy-Revised (SIS-R) was administered to analyse scores of total, positive, and negative schizotypy in siblings and healthy comparison participants. The PRS-SCZ was trained using the Psychiatric Genomics Consortiums results and the ES-SCZ was calculated guided by the approach validated in a previous report in the current data set. Regression models were applied to test the independent and joint effects of PRS-SCZ and ES-SCZ (adjusted for age, sex, and ancestry using 10 principal components).

Both genetic and environmental vulnerability were associated with case-control status. Furthermore, there was evidence for additive interaction between binary modes of PRS-SCZ and ES-SCZ (above 75% of the control distribution) increasing the odds for schizophrenia spectrum diagnosis (relative excess risk due to interaction = 6.79, [95% confidential interval (CI) 3.32, 10.26], p < 0.001). Sensitivity analyses using continuous PRS-SCZ and ES-SCZ confirmed gene–environment interaction (relative excess risk due to interaction = 1.80 [95% CI 1.01, 3.32], p = 0.004). In siblings and healthy comparison participants, PRS-SCZ and ES-SCZ were associated with all SIS-R dimensions and evidence was found for an interaction between PRS-SCZ and ES-SCZ on the total (B = 0.006 [95% CI 0.003, 0.009], p < 0.001), positive (B = 0.006 [95% CI, 0.002, 0.009], p = 0.002), and negative (B = 0.006, [95% CI 0.004, 0.009], p < 0.001) schizotypy dimensions.

The interplay between exposome load and schizophrenia genetic liability contributing to psychosis across the spectrum of expression provide further empirical support to the notion of aetiological continuity underlying an extended psychosis phenotype.

There is evidence that environmental and genetic risk factors for schizophrenia spectrum disorders are transdiagnostic and mediated in part through a generic pathway of affective dysregulation.

We analysed to what degree the impact of schizophrenia polygenic risk (PRS-SZ) and childhood adversity (CA) on psychosis outcomes was contingent on co-presence of affective dysregulation, defined as significant depressive symptoms, in (i) NEMESIS-2 (n = 6646), a representative general population sample, interviewed four times over nine years and (ii) EUGEI (n = 4068) a sample of patients with schizophrenia spectrum disorder, the siblings of these patients and controls.

The impact of PRS-SZ on psychosis showed significant dependence on co-presence of affective dysregulation in NEMESIS-2 [relative excess risk due to interaction (RERI): 1.01, p = 0.037] and in EUGEI (RERI = 3.39, p = 0.048). This was particularly evident for delusional ideation (NEMESIS-2: RERI = 1.74, p = 0.003; EUGEI: RERI = 4.16, p = 0.019) and not for hallucinatory experiences (NEMESIS-2: RERI = 0.65, p = 0.284; EUGEI: −0.37, p = 0.547). A similar and stronger pattern of results was evident for CA (RERI delusions and hallucinations: NEMESIS-2: 3.02, p < 0.001; EUGEI: 6.44, p < 0.001; RERI delusional ideation: NEMESIS-2: 3.79, p < 0.001; EUGEI: 5.43, p = 0.001; RERI hallucinatory experiences: NEMESIS-2: 2.46, p < 0.001; EUGEI: 0.54, p = 0.465).

The results, and internal replication, suggest that the effects of known genetic and non-genetic risk factors for psychosis are mediated in part through an affective pathway, from which early states of delusional meaning may arise.

This study attempted to replicate whether a bias in probabilistic reasoning, or ‘jumping to conclusions’(JTC) bias is associated with being a sibling of a patient with schizophrenia spectrum disorder; and if so, whether this association is contingent on subthreshold delusional ideation.

Data were derived from the EUGEI project, a 25-centre, 15-country effort to study psychosis spectrum disorder. The current analyses included 1261 patients with schizophrenia spectrum disorder, 1282 siblings of patients and 1525 healthy comparison subjects, recruited in Spain (five centres), Turkey (three centres) and Serbia (one centre). The beads task was used to assess JTC bias. Lifetime experience of delusional ideation and hallucinatory experiences was assessed using the Community Assessment of Psychic Experiences. General cognitive abilities were taken into account in the analyses.

JTC bias was positively associated not only with patient status but also with sibling status [adjusted relative risk (aRR) ratio : 4.23 CI 95% 3.46–5.17 for siblings and aRR: 5.07 CI 95% 4.13–6.23 for patients]. The association between JTC bias and sibling status was stronger in those with higher levels of delusional ideation (aRR interaction in siblings: 3.77 CI 95% 1.67–8.51, and in patients: 2.15 CI 95% 0.94–4.92). The association between JTC bias and sibling status was not stronger in those with higher levels of hallucinatory experiences.

These findings replicate earlier findings that JTC bias is associated with familial liability for psychosis and that this is contingent on the degree of delusional ideation but not hallucinations.

Compulsory admission procedures of patients with mental disorders vary between countries in Europe. The Ethics Committee of the European Psychiatric Association (EPA) launched a survey on involuntary admission procedures of patients with mental disorders in 40 countries to gather information from all National Psychiatric Associations that are members of the EPA to develop recommendations for improving involuntary admission processes and promote voluntary care.

The survey focused on legislation of involuntary admissions and key actors involved in the admission procedure as well as most common reasons for involuntary admissions.

We analyzed the survey categorical data in themes, which highlight that both medical and legal actors are involved in involuntary admission procedures.

We conclude that legal reasons for compulsory admission should be reworded in order to remove stigmatization of the patient, that raising awareness about involuntary admission procedures and patient rights with both patients and family advocacy groups is paramount, that communication about procedures should be widely available in lay-language for the general population, and that training sessions and guidance should be available for legal and medical practitioners. Finally, people working in the field need to be constantly aware about the ethical challenges surrounding compulsory admissions.

Stigmatization of a psychiatric patient is present both in general population and among health-care professionals.

To determine the attitudes of medical students (MS) towards a person who goes to a psychiatrist, before and after psychiatric rotation, and to compare those attitudes between medical and non-medical students.

The study included 525 MS (2nd and 6th year of studies) and 154 students of law. The study instrument was a 3-part self-reported questionnaire (socio-demographic data, Rosenberg self-esteem scale and a vignette depicting young, mentally healthy person). The experimental intervention consisted of ascribing a “psychiatric label” to only one set of vignettes. All the vignettes (with or without “psychiatric label”) were followed by 14 statements addressing acceptance of a person described by vignette as judged by social distance.

We found more stigmatizing attitudes of the MS in the final year, after psychiatric rotation. The non-medical students had similar tendency to stigmatize as MS before psychiatric rotation. A higher level of stigmatization was evident in regard to a closer relationship between a student and a hypothetic person who goes to a psychiatrist. Neither sex, nor the size of student's place of origin or average academic mark was associated with the tendency to stigmatize.

Psychiatric education can either reinforce stigma or reduce it. Therefore, detailed analyses of educational domains which reinforce stigma should be conducted at the university level, in parallel with national initiative to fight against stigma and discrimination attached to mental health problems and those living with them.

The core mechanism of maladaptive stress response includs aberrant phosphorylation of the glucocorticoid receptor (GR) at serine 221 (pGR211) or GR serine 226 (pGR226), which enhance or attenuate GR transcriptional activity, respectively. In the current study we tested a hypothesis that alterations in the nuclear levels and/or ratios of GR, pGR211 and pGR226 in peripheral blood mononuclear cells (PBMC) may reflect individual level of distress and/or psychological vulnerability.

In 36 healthy adults we evaluated the relation of total PMBC nuclear level of GR (tGR), pGR221, pGR226 and activated JNK1 (pJNK1) and its relation to environmental stress exposure, self reported distress (Depression Anxiety Stress Scale) and personality traits (Eysenck Personality Questionnaire). Molecular and psychometric data were cross-correlated by SPSS MannWhitney statistics.

In women, self reported distress (DASS score) correlated more with neuroticism, while in men it correlated with environmental stressor. Also, in women, PBMC nuclear tGR level correlated with pGR211, while in men it correlated with pGR226. Cross-analysis of psychometric and molecular data indicated that in women both neuroticism and self reported distress correlated positively with nuclear pGR226, while in men the only correlation was between environmental stressor and pJNK1.

This findings provide preliminary support that the nuclear level of pGR226 and pGR211/pGR226 ratio in PBMC may serve as a measure of affective vulnerability in healthy women, while nuclear level of pJNK1 may reflect environmentaly imposed distress in healthy men. The relevance of these molecular parameters as biomarkers requires broader verification in healthy and in clinical settings.

Current knowledge about the advantages of using split version of GAF scale – having separate Symptom (GAF-S) and Functioning (GAF-F) subscales is insufficient and has number of gaps. Present study analyzed the manner in which young adult remitted psychotic patients with different functional levels vary in their symptom severity and how GAF-F reflects presence/absence of well-known psychosis risk factors.

Sample comprised 37 remitted psychotic patients (56.8% male, 29.4 ± 6.1 years), categorized based on GAF-F scores into groups: ‘Moderate remission’ (GAF-F 41–60, n = 19) and “Good remission” (GAF-F > 61, n = 18). Participants were assessed using the GAF-S, WAIS-R, Nottingham Onset Schedule, Premorbid Adjustment and Brief Core Schema scales, childhood trauma and bullying questionnaires. Mann–Whitney and Student's t-tests were used to assess between-group differences.

Groups did not differ in age, sex and education. When compared to “Good remission” group, “Moderate remission” group exhibited earlier illness’ onset (P = 0.01), greater symptom severity (P = 0.00), negative self-evaluation (P = 0.02), more childhood physical abuse (P = 0.01) and bullying (P = 0.01). Moreover, trend-like significances (P = 0.08) were observed for poorer adolescence adjustment and negative evaluation of others. There were no between-group differences regarding IQ and duration of untreated/treated illness.

GAF scale is in the continual use since early 1990, however, evidence of further development of the instrument itself is sparse. Present research is demonstrating that GAF-F scores reflect diverse factors related to psychosis risk, the illness’ course and quality of remission. Moreover, the results contribute to surmount some of the gaps in knowledge about the split version of GAF scale.

The authors have not supplied their declaration of competing interest.

Ubiquitous negative emotional states such as depression, anxiety and stress in adulthood are related to individual life scenario, particularly influenced by exposure to environmental risk factors. Here, we investigated if sub-threshold negative emotional states in general population can be predicted by experience of trauma in the childhood.

A sample of 106 healthy young adult participants from Belgrade and surroundings (43.4% male, age 29.2 ± 6.6 years, mean IQ 106.4 ± 15.9) fulfilled Childhood Trauma Questionnaire (CTQ) to identify emotional or physical abuse/neglect or sexual abuse. Present level of negative affectivity was measured by Depression Anxiety Stress Scale (DASS). Hierarchical linear regression analysis was conducted to identify subtypes of trauma as predictors of the negative affectivity.

Mean CTQ and DASS scores were 31.2 ± 6.7 and 16.4 ± 16.8, respectively. An exposure to given risk factors in the past correlated significantly with intensity of the present negative affective states (r = 0.290, P = 0.004). For the prediction of anxiety, the most important traumatism subtypes were emotional abuse, emotional neglect and physical abuse (P = 0.001; 0.028; and 0.041, respectively). Depressive symptoms were predicted only by the emotional abuse in the past (P = 0.008).

Based on clinical samples, findings from the literature yielded greater risk for mood and anxiety disorders after exposure to emotional, in comparison to the physical trauma. We confirmed the same pattern of correlations in the healthy subject's sample, who had no history mental disorders. Evaluation of the interaction effects among emotional trauma and genotype is strongly recommended in the identification of subjects at risk and for the prevention.

The authors have not supplied their declaration of competing interest.

Electroconvulsive therapy (ECT) has been considered a treatment option for the treatment resistance, mania, depression, suicidality and schizophrenia. It has been still controversial due to the lack of controlled clinical trials and unknown biological basis but also because of the negative image from the history of the treatment.

Specifics of the clinical judgement on when and for which patients’ indications, ECT was a treatment choice.

Aim of the study was to evaluate indications for the ECT treatment in the hospitalized psychiatric patients at the psychiatric department.

For all the patient cases in the last 7 years at the department (n = 326), data was analyzed regarding age, gender, number of hospitalizations, age of first episode, diagnose, previous treatment, leading indication for ECT and outcome after the ECT, regarding following treatment.

The leading indication for ECT was psychosis and/or pharmacological treatment resistance, followed by suicidality. Patients with psychosis were younger than patients with other diagnoses when receiving ECT treatment. Regarding the results, indications for ECT had been partially differentiated from expected guidelines. Outcomes after the ECT were favorable in terms of better controlling the symptoms, lowering exacerbation frequency and intensity and partially, functioning.

Studies on ECT indications and outcome could provide further insight on efficacy of the treatment, and possible improvements in clinical assessment on eligible patients who could benefit from the ECT treatment.

The authors have not supplied their declaration of competing interest.

Previous studies suggested that patients with schizophrenia had an increased prevalence of antibodies against toxoplasma gondii (TG) and that those seropositive patients had higher symptom severity. However, there is no data on the relationship between treatment-resistant schizophrenia (TRS) and TG seroprevalence.

To determine the association between TRS and TG seropositivity, and to further investigate the relationship between TG seropositivity and different clinical features of schizophrenia.

In this cross-sectional study, we included 210 male inpatients with schizophrenia. TG seropositivity was determined by ELFA assay. Treatment-resistance was defined as a failure of at least 2 adequate anti-psychotic trials. Data were analyzed using χ2 test or Mann–Whitney test.

The rate of TG seropositivity in the entire sample was 52.3%, whereas 47.6% of patients met the definition for treatment-resistance. Seropositive patients had twice the rate of treatment–resistance compared to seronegative patients (63.6% vs. 30.0%, P < 0.0001). Moreover, in the seropositive group, the patients were older (47.6 ± 12.2 vs. 39.81 ± 12.01 years, P < 0.0001), had higher number of previous hospitalizations (13.9 ± 11.7 vs. 9.6 ± 8.5, P = 0.0073), and increased Calgary depression scale for schizophrenia (CDSS) total score (7.8 ± 4.5 vs. 6.3 ± 3.8, P = 0.012). There were no differences between the groups in the age of disease onset, smoking, positive and negative syndrome scale (PANSS) total, positive and negative scores, and the life-time history of suicide attempts.

Our results support the hypothesis that TG seropositivity might contribute to treatment-resistance in schizophrenia, at least in male patients.

The authors have not supplied their declaration of competing interest.

Treatment with pegylated interferon alpha (PEG-IFN-α) in patients with chronic hepatitis C (CHC) is associated with depressive symptomatology more frequently than other inflammatory diseases treated with PEG-IFN-α.

To prospectively evaluate the onset, course and resolution of depressive symptomatology in CHC patients treated with PEG-IFN-α.

Hamilton depression rating scale (HAMD) was used to asses depressive symptoms in 103 subjects with CHC prior to initiation of PEG-IFN-α (mean dose 152.6 ± 25.6 mcg; duration of therapy 48 weeks) and at the follow-up visits (4th, 12th, 24th, 48th and 72th week). Control group consisted of 103 CHC subjects, without PEG-IFN-α.

Our results showed a significant increase in HAMD scores as early as in the 4th week of PEG-IFN-a therapy compared to HAMD scores prior to initiation of PEG-IFN-α (38.8% vs. 24.3%). The peak of depressive symptomatology was evidenced in the 12th week (mean HAMD 9.34 ± 6.93), when almost 50% of patients had HAMD above 7. At the end of the treatment (48th week), 38.8% had HAMD above 7, and in the 72nd week (24 weeks after the therapy completion) prevalence of depression was decreased to the values lower than at baseline (23.3% vs. 24.3%). No change in prevalence of depression was detected in control group.

Our results are important because they show the overall course of depressive symptomatology during the interferon therapy. These data also show spontaneously resolution of depression 6 months after the completion of PEG-IFN-α. This study is the longest study in this area.

The authors have not supplied their declaration of competing interest.

First-degree relatives of patients with psychotic disorder have higher levels of polygenic risk (PRS) for schizophrenia and higher levels of intermediate phenotypes.

We conducted, using two different samples for discovery (n = 336 controls and 649 siblings of patients with psychotic disorder) and replication (n = 1208 controls and 1106 siblings), an analysis of association between PRS on the one hand and psychopathological and cognitive intermediate phenotypes of schizophrenia on the other in a sample at average genetic risk (healthy controls) and a sample at higher than average risk (healthy siblings of patients). Two subthreshold psychosis phenotypes, as well as a standardised measure of cognitive ability, based on a short version of the WAIS-III short form, were used. In addition, a measure of jumping to conclusion bias (replication sample only) was tested for association with PRS.

In both discovery and replication sample, evidence for an association between PRS and subthreshold psychosis phenotypes was observed in the relatives of patients, whereas in the controls no association was observed. Jumping to conclusion bias was similarly only associated with PRS in the sibling group. Cognitive ability was weakly negatively and non-significantly associated with PRS in both the sibling and the control group.

The degree of endophenotypic expression of schizophrenia polygenic risk depends on having a sibling with psychotic disorder, suggestive of underlying gene–environment interaction. Cognitive biases may better index genetic risk of disorder than traditional measures of neurocognition, which instead may reflect the population distribution of cognitive ability impacting the prognosis of psychotic disorder.