World Journal of Biological Psychiatry最新文献

Objectives: We used machine learning to incorporate three types of biomarkers (respiratory sinus arrhythmia, RSA; skin conductance, SC; finger temperature, FT) for examining the performance of diagnosing somatic symptom disorder (SSD).

Methods: We recruited 97 SSD subjects and 96 controls without psychiatric history or somatic distress. The values of RSA, SC and FT were recorded in three situations (resting state, under a cognitive task and under paced breathing) and compared for the two populations. We used machine learning to combine the biological signals and then applied receiver operating characteristic curve analysis to examine the performance of diagnosing SSD regarding the distinct indicators and situations. Subgroup analysis for subjects without depression/anxiety was also conducted.

Results: FT was significantly different between SSD patients and controls, especially in the resting state and under paced breathing. However, the biomarkers (0.75-0.76) did not reveal an area under the curve (AUC) comparable with the psychological questionnaires (0.86). Combining the biological and psychological indicators gave a high AUC (0.86-0.92). When excluding individuals with depression/anxiety, combining three biomarkers (0.79-0.83) and adopting psychological questionnaires (0.78) revealed a similar AUC.

Conclusions: The performance of RSA/SC/FT was unsatisfactory for diagnosing SSD but became comparable when excluding comorbid depression/anxiety.

Background: Agomelatine is a melatoninergic antidepressant approved to treat the major depressive disorder. Agomelatine exerts its behavioural, pharmacological, and physiological effects through the activation of MT₁ and MT₂ melatonin receptors and the blockade of 5-HT_2B and 5-HT_2C serotonin receptors. Some studies have reported that the activation of the MT₁ and MT₂ melatonin receptors decreased cocaine-induced locomotor activity and cocaine self-administration. These findings from another study showed that agomelatine decreased alcohol consumption. This study aimed to evaluate the effects of agomelatine administration on cocaine-induced behavioural (cocaine-induced locomotor activity and cocaine-induced locomotor sensitisation) and neurochemical (dopamine levels) effects.

Methods: Male Wistar rats (250-280 g) received cocaine (10 mg/kg) during the induction and expression of locomotor sensitisation. Agomelatine (10 mg/kg) was administered 30 minutes before cocaine. After each treatment, locomotor activity was recorded for 30 minutes. Dopamine levels were determined in the ventral striatum, the prefrontal cortex (PFC), and the ventral tegmental area (VTA) by high-performance liquid chromatographic (HPLC) in animals treated with agomelatine and cocaine. Luzindole (30 mg/kg) was administered to block the agomelatine effect.

Results: In this study, we found that agomelatine decreased cocaine-induced locomotor activity and the induction and expression of locomotor sensitisation. In addition, agomelatine decreased cocaine-induced dopamine levels. Luzindole blocked the agomelatine-induced decrease in the expression of locomotor sensitisation in rats.

Conclusion: Our results suggest (1) that agomelatine showed efficacy in decreasing cocaine psychostimulant effects and (2) that agomelatine can be a useful therapeutic agent to reduce cocaine abuse.

Objectives: This 2023 update of the WFSBP guidelines for the pharmacological treatment of eating disorders (EDs) reflects the latest diagnostic and psychopharmacological progress and the improved WFSBP recommendations for the assessment of the level of evidence (LoE) and the grade of recommendation (GoR).

Methods: The WFSBP Task Force EDs reviewed the relevant literature and provided a timely grading of the LoE and the GoR.

Results: In anorexia nervosa (AN), only a limited recommendation (LoE: A; GoR: 2) for olanzapine can be given, because the available evidence is restricted to weight gain, and its effect on psychopathology is less clear. In bulimia nervosa (BN), the current literature prompts a recommendation for fluoxetine (LoE: A; GoR: 1) or topiramate (LoE: A; GoR: 1). In binge-eating disorder (BED), lisdexamfetamine (LDX; LoE: A; GoR: 1) or topiramate (LoE: A; GoR: 1) can be recommended. There is only sparse evidence for the drug treatment of avoidant restrictive food intake disorder (ARFID), pica, and rumination disorder (RD).

Conclusion: In BN, fluoxetine, and topiramate, and in BED, LDX and topiramate can be recommended. Despite the published evidence, olanzapine and topiramate have not received marketing authorisation for use in EDs from any medicine regulatory agency.

Objectives: To summarise SNP associations identified by genome-wide association studies (GWASs) of anxiety disorders and neuroticism; to appraise the quality of individual studies, and to assess the ancestral diversity of study participants.

Methods: We searched PubMed, Scopus, PsychInfo and PubPsych for GWASs of anxiety disorders, non-diagnostic traits (such as anxiety sensitivity), and neuroticism, and extracted all SNPs that surpassed genome-wide significance. We graded study quality using Q-genie scores and reviewed the ancestral diversity of included participants.

Results: 32 studies met our inclusion criteria. A total of 563 independent significant variants were identified, of which 29 were replicated nominally in independent samples, and 3 were replicated significantly. The studies had good global quality, but many smaller studies were underpowered. Phenotypic heterogeneity for anxiety (and less so for neuroticism) seemed to reflect the complexity of capturing this trait. Ancestral diversity was poor, with 70% of studies including only populations of European ancestry.

Conclusion: The functionality of genes identified by GWASs of anxiety and neuroticism deserves further investigation. Future GWASs should have larger sample sizes, more rigorous phenotyping and include more ancestrally diverse population groups.

Objectives: This study attempts to assess the concentration of two opposite-acting adipokines (anti-inflammatory adiponectin and pro-inflammatory resistin) in antidepressant-resistant patients undergoing ketamine infusion (KI) and electroconvulsive therapy (ECT).

Methods: The study group comprised 52 patients hospitalised due to episodes of depression in the course of bipolar disorders. The Hamilton depression scale was used to assess the intensity of the depression symptoms before starting therapy and one day after its completion. The serum concentration of adipokines was determined before and after the therapeutic intervention using an ELISA method.

Results: Baseline adipokine levels differed between patients receiving KI and ECT therapy. Regardless of the procedure used, these levels changed after treatment, with the nature of these changes being different. In the case of KI, the adiponectin levels increased, and resistin levels decreased. In contrast, after ECT, the concentrations of both adipokines decreased. Changes in adipokine concentrations correlated with improvement in mental status, as assessed by the Hamilton Rating Scale, type of bipolar disorder, and gender.

Conclusions: Adipokines remain interesting candidate biomarkers in assessing the state and course of the disease depending on the therapeutic procedure applied. However, the relatively small study group and limited original research available for discussion justify further investigation.

Objective: P-type atypical lymphocytes may play important roles in the aetiology and therapy of schizophrenia. However, there is merely a direct immunological characterisation of it. The aim of this study is to explore the surface antigens of these cells and their comparative ultrastructure in schizophrenia.

Methods: We recruited 25 age-and gender-matched patients with unmedicated schizophrenia, other mental diseases and healthy individuals. Peripheral venous blood was smeared and stained. CD4+, CD8+ and CD19+ cell surface antigen- positive lymphocytes were purified using magnetic beads and prepared for light microscopy and electron microscopy.

Results: The percentages of P-type atypical lymphocytes (34.53% ± 9.92%) were significantly higher (p < 0.0001) in schizophrenia than that of other mental diseases (9.79% ± 3.45%). These cells could present CD4+, CD8+ and CD19+ surface antigens. Their relative ultrastructure differed from that of normal lymphocytes, especially in mitochondria, which showed abundant, aggregated and quite irregular mitochondria; for example, slight dilation of the foci, swelling, degeneration, and even cavity.

Conclusions: P-type atypical lymphocytes could be found among CD4+, CD8+, and CD19 + lymphocytes with schizophrenia. Their abnormal ultrastructure of mitochondria implied that energy metabolism might play an important role in the aetiology of schizophrenia.

Objectives: Obsessive-compulsive disorder (OCD) can rarely be associated with immunological aetiologies, most notably in Paediatric Autoimmune Neuropsychiatric Disorder Associated with Streptococcal Infections and possibly in autoimmune encephalitis. As cerebrospinal fluid (CSF) analysis is a sensitive method for assessing neuroinflammation, this retrospective study analysed basic CSF parameters and well-characterised as well as novel neuronal autoantibodies in OCD to screen for signs of autoimmunity.

Methods: Basic CSF findings of 54 adult OCD patients suspected of an organic aetiology were retrospectively compared to a control group of mentally healthy patients (N = 39) with idiopathic intracranial hypertension. Further subgroup analysis included testing for well-characterised neuronal IgG autoantibodies and tissue-based assays using indirect immunofluorescence to screen for novel brain autoantibodies.

Results: Elevated protein in the CSF of OCD patients compared to the control group (p = 0.043) was identified. Inflammatory markers (pleocytosis/oligoclonal bands/increased IgG-index) were detected in 7% of all patients with OCD. Well-characterised neuronal autoantibodies were not found in any OCD patient, whereas 6/18 (33%) CSF samples showed binding on mouse brain sections in tissue-based assays (binding to neuropil in the basal ganglia/brainstem, cilia of granule cells, blood vessels, nuclear/perinuclear structures).

Conclusions: While elevated CSF protein is merely a weak indicator of blood CSF barrier dysfunction, the presence of inflammatory CSF changes and novel brain autoantibodies in CSF may indicate OCD subtypes with inflammatory pathomechanism and supports the hypothesis of a rare "autoimmune OCD" subtype.

Objectives: The endocannabinoid system (ECS) is a critical important neuromodulatory system that interacts with many neurohormonal and neurotransmitter systems in the brain. It plays a pivotal role in emotional responses and mood regulation. The ECS is related with psychotic disorders, depression, anxiety and autism. In this study, we aimed to investigate whether there is any relationship between endocannabinoid and N-acylethanolamine levels with bipolar disorder.

Methods: Seventy-nine patients with bipolar disorder diagnosis, who are in the euthymic period, were included in the study. Clinical characteristics, symptoms and serum endocannabinoid and N-acylethanolamine levels were compared. Endocannabinoid and N-acylethanolamine levels were evaluated using liquid chromatography-tandem mass spectrometry.

Results: In total of 79 patients, 44 (55.69%) were females and 35 (44.30%) were males. The mean age of the patients was 42.40 ± 1.10 years. Palmitoylethanolamide (PEA) levels were higher and oleoylethanolamide and 2-arachidonyl glycerol levels were lower in patients who had at least one depressive episode during their life-time illness than in patients who had no depressive episode while arachidonyl ethanolamide levels were unchanged.

Conclusions: PEA levels were correlated with the history and frequency of depressive episodes and the history of depressive symptoms in patients with bipolar disorder.

Objectives: Recently, the expression changes of microRNAs (miRNAs) in the serum exosomes (EXO) of schizophrenia (SCZ) have been reported. The aim of this study was to investigate the global expression changes of miRNA derived from the plasma EXO of patients with treatment-resistant schizophrenia (TRS) and the effects of clozapine on miRNA expression.

Methods: Global miRNA expression changes in plasma EXO between TRS and controls were studied using microarray analysis. Then, miRNA expressions among TRS, non-TRS, and controls were confirmed with quantitative qPCR experiments. We also studied changes in EXO miRNA expression with in-vitro SH-SY5Y cells.

Results: A microarray for miRNA expression analysis (nine controls vs. nine patients with TRS) revealed 13 up- and 18 downregulated miRNAs that were relevant to neuronal and brain development based on gene ontology analysis. Of those, upregulated miR-675-3p expression was successfully validated in the same cohort by qPCR experiments. Conversely, miR-675-3p expression levels were significantly decreased in the non-TRS cohort (50 controls vs. 50 patients without TRS without clozapine treatment).

Conclusions: We identified global miRNA changes in plasma EXO derived from patients with SCZ that were relevant to neuronal functions, among which, hsa-miR-675-3p expression was upregulated by clozapine treatment.