World Journal of Biological Psychiatry最新文献

Objectives: Melancholia is a severe form of depression that is typified by greater genetic and biological influence, distinct symptomatology, and preferential response to physical treatment. This paper sought to broadly overview potential biomarkers of melancholia to benefit differential diagnosis, clinical responses and treatment outcomes. Given nuances in distinguishing melancholia as its own condition from other depressive disorder, we emphasised studies directly comparing melancholic to non-melancholic depression.

Methods: A comprehensive literature search was conducted. Key studies were identified and summarised qualitatively.

Results: 105 studies in total were identified. These studies covered a wide variety of biomarkers, and largely fell into three domains: endocrinological (especially cortisol levels, particularly in response to the dexamethasone suppression test), neurological, and immunological (particularly inflammatory markers). Less extensive evidence also exists for metabolic, genetic, and cardiovascular markers.

Conclusions: Definitive conclusions were predominantly limited due to substantial heterogeneity in how included studies defined melancholia. Furthermore, this heterogeneity could be responsible for the between- and within-group variability observed in the candidate biomarkers that were examined. Therefore, clarifying these definitional parameters may help identify underlying patterns in biomarker expression to improve diagnostic and therapeutic precision for the depressive disorders.

Objectives: Borderline personality disorder (BPD) and bipolar disorder (BD) often co-occur and frequently do not respond adequately to traditional antidepressant treatments. Ketamine has shown rapid antidepressant and anti-suicidal effects. However, there is limited literature on the safety and tolerance of using ketamine to treat patients with comorbid BD and BPD.

Methods: This case presents a female patient diagnosed with both Bipolar Disorder (BD) and Borderline Personality Disorder (BPD) who received intravenous ketamine treatment to alleviate acute depressive symptoms.

Results: Initially, ketamine ameliorated depressed symptoms. However, as the ketamine treatment continued, the patient showed an increase in nonsuicidal self-injury (NSSIs) and impulsive conduct with a aggravation of dissociative symptoms. As a result, intravenous ketamine was discontinued, and the patient received the medication, which proved helpful.

Conclusions: Although ketamine presents antidepressant properties, reports on its impact on emotional dysregulation and impulsive conduct are unclear and not alike to its antidepressant effect. Therefore, there is a need for more studies investigating the effectiveness and safety of this rapid-acting medicine in this patient population.

Objectives: Major depression (MD) may be associated with inflammation and immunity. PD-1 (programmed death-1), PD-L1 (programmed death-ligand 1) and PD-L2 (programmed death-ligand 2) are among the inhibitory immune mediators on the PD-1 pathway. However, previous data regarding the association between MD and PD-1 pathway were still scarce; therefore, we investigated the association of PD-1 pathway with MD.

Methods: During a period of 2 years, patients with MD and healthy controls were recruited from a medical centre in this study. The diagnosis of MD was established according to the DSM-5 criteria. The severity of MD was assessed with 17-item Hamilton Depression Rating Scale. PD-1, PD-L1 and PD-L2 were detected in peripheral blood from MD patients after 4 weeks of treatment with antidepressant drugs.

Results: A total of 54 patients with MD and 38 healthy controls were recruited. According to the analyses, there is a significantly higher PD-L2 level in MD than in healthy controls and lower PD-1 level after age and BMI adjustment. Besides, moderately positive correlation between HAM-D scores and PD-L2 level was found.

Conclusions: It was found that PD-1 pathway might play an important role in MD. We need a large sample to prove these results in the future.

Objectives: Schizophrenia is a chronic, debilitating mental disorder whose pathophysiology is complex and not fully understood. Numerous studies suggest mitochondrial dysfunction may contribute to the development of schizophrenia. While mitochondrial ribosomes (mitoribosomes) are essential for proper mitochondrial functioning, their gene expression levels have not been studied yet in schizophrenia.

Methods: We performed a systematic meta-analysis of the expression of 81 mitoribosomes subunits encoding genes, integrating ten brain samples datasets of patients with schizophrenia compared to healthy controls (overall 422 samples, 211 schizophrenia, and 211 controls). We also performed a meta-analysis of their expression in blood, integrating two blood sample datasets (overall 90 samples, 53 schizophrenia, and 37 controls).

Results: Multiple mitoribosomes subunits were significantly downregulated in brain samples (18 genes) and in blood samples (11 genes) of individuals with schizophrenia, where two showed significant downregulation in both brain and blood, MRPL4 and MRPS7.

Conclusions: Our results support the accumulating evidence of impaired mitochondrial activity in schizophrenia. While further research is needed to validate mitoribosomes' role as biomarkers, this direction has the potential to promote patients' stratification and personalised treatment for schizophrenia.

Objectives: Brain-derived neurotrophic factor (BDNF) levels vary in various conditions including alcohol use disorder (AUD). We aimed to identify drivers of these variations.

Methods: Twelve patients with AUD were assessed at hospitalisation for alcohol withdrawal and four months later. We looked for associations between the change in serum BDNF levels and (1) length of abstinence, (2) anxiety (Hamilton Anxiety Scale) and depression (Beck-Depression Inventory), (3) one functional BDNF genotype (rs6265) and (4) methylation levels of 12 CpG sites within the BDNF gene (located in exons I, IV and IX).

Results: While abstinence remained, serum BDNF level increased. This increase correlated with the variation of methylation levels of the BDNF gene, and more specifically of exon I. We found no significant effect of length of abstinence, rs6265, depression or anxiety on serum BDNF level.

Conclusions: Epigenetic regulation of the BDNF gene may be involved in variations of BDNF blood level associated with alcohol abstinence.

Objectives: Due to the common neurodevelopmental origin and easy accessibility, the retina serves as a surrogate marker for changes in the brain. Hence, Optical Coherence Tomography (OCT), a tool to examine the neuronal layers of retina has gained importance in investigating psychiatric disorders. Several studies in the last decade have reported retinal structural alterations in schizophrenia (SCZ), bipolar disorder (BD), and major depressive disorder (MDD). However, the findings are inconsistent. Hence, we conducted a meta-analysis to investigate alterations in OCT parameters in patients with SCZ, BD and MDD.

Methods: We searched electronic databases for studies that examined OCT parameters in patients with SCZ, BD and MDD published up to January 2023. The primary outcome measures were thickness and volumes of the retinal Nerve Fibre Layer (RNFL). We conducted meta-analysis using a random effects model.

Results: The searches yielded 2638 publications of which 43 studies were included in the final analysis across all disorders. Compared to controls, the RNFL was thinner in SCZ patients (SMD = -0.37, p = <0.001) and BD patients (SMD = -0.67, p = < 0.001), but not in MDD patients (SMD = -0.08, p = 0.54). On quadrant wise analysis, temporal quadrant RNFL was thinner in SCZ but not in BD, while all other quadrants were thinner in both SCZ and BD.

Conclusion: We found significant reductions in RNFL thickness in SCZ and BD, but not in MDD. The differential involvement in various quadrants and parameters across the disorders has potential implications for using retinal parameters as a diagnostic biomarker.

Objectives: Schizophrenia is characterised by deficits across multiple cognitive domains and altered glutamate related neuroplasticity. The purpose was to investigate whether glutamate deficits are related to cognition in schizophrenia, and whether glutamate-cognition relationships are different between schizophrenia and controls.

Methods: Magnetic resonance spectroscopy (MRS) at 3 Tesla was acquired from the dorsolateral prefrontal cortex (dlPFC) and hippocampus in 44 schizophrenia participants and 39 controls during passive viewing visual task. Cognitive performance (working memory, episodic memory, and processing speed) was assessed on a separate session. Group differences in neurochemistry and mediation/moderation effects using structural equation modelling (SEM) were investigated.

Results: Schizophrenia participants showed lower hippocampal glutamate (p = .0044) and myo-Inositol (p = .023) levels, and non-significant dlPFC levels. Schizophrenia participants also demonstrated poorer cognitive performance (p < .0032). SEM-analyses demonstrated no mediation or moderation effects, however, an opposing dlPFC glutamate-processing speed association between groups was observed.

Conclusions: Hippocampal glutamate deficits in schizophrenia participants are consistent with evidence of reduced neuropil density. Moreover, SEM analyses indicated that hippocampal glutamate deficits in schizophrenia participants as measured during a passive state were not driven by poorer cognitive ability. We suggest that functional MRS may provide a better framework for investigating glutamate-cognition relationships in schizophrenia.

Objectives: Schizophrenia (SZ) and intellectual disability (ID) are both included in the continuum of neurodevelopmental disorders (NDDs). DNA methylation is known to be important in the occurrence of NDDs. The family study is conducive to eliminate the effects of relative epigenetic backgrounds, and to screen for differentially methylated positions (DMPs) and regions (DMRs) that are truly associated with NDDs.

Methods: Four monozygotic twin families were recruited, and both twin individuals suffered from NDDs (either SZ, ID, or SZ plus ID). Genome-wide methylation analysis was performed in all samples and each family. DMPs and DMRs between NDD patients and unaffected individuals were identified. Functional and pathway enrichment analyses were performed on the annotated genes.

Results: Two significant DMPs annotated to CYP2E1 were found in all samples. In Family One, 1476 DMPs mapped to 880 genes, and 162 DMRs overlapping with 153 unique genes were recognised. Our results suggested that the altered methylation levels of FYN, STAT3, RAC1, and NR4A2 were associated with the development of SZ and ID. Neurodevelopment and the immune system may participate in the occurrence of SZ and ID.

Conclusions: Our findings suggested that DNA methylation participated in the development of NDDs by affecting neurodevelopment and the immune system.

Objectives: Thus far, the diagnosis of insomnia is based on purely clinical criteria. Although a broad range of altered physiological parameters has been identified in insomniacs, the evidence to establish their diagnostic usefulness is very limited. Purpose of this WFSBP Task Force consensus paper is to systematically evaluate a series of biomarkers as potential diagnostic tools for insomnia.

Methods: A newly created grading system was used for assessing the validity of various measurements in establishing the diagnosis of insomnia; these measurements originated from relevant studies selected and reviewed by experts.

Results: The measurements with the highest diagnostic performance were those derived from psychometric instruments. Biological measurements which emerged as potentially useful diagnostic instruments were polysomnography-derived cyclic alternating pattern, actigraphy, and BDNF levels, followed by heart rate around sleep onset, deficient melatonin rhythm, and certain neuroimaging patterns (mainly for the activity of frontal and pre-frontal cortex, hippocampus and basal ganglia); yet, these findings need replication, as well as establishment of commonly accepted methodology and diagnostic cut-off points. Routine polysomnography, EEG spectral analysis, heart rate variability, skin conductance, thermoregulation, oxygen consumption, HPA axis, and inflammation indices were not shown to be of satisfactory diagnostic value.

Conclusions: Apart from psychometric instruments which are confirmed to be the gold standard in diagnosing insomnia, six biomarkers emerge as being potentially useful for this purpose.

Objectives: Despite the increasingly high prevalence and serious consequences of depression in adolescents, there is a lack of economical and reliable biomarkers to aid the diagnostic process. Recent findings suggest that red blood cell distribution width (RDW) is an easily obtainable biomarker of depression in adults. Here, we aimed to replicate the finding of increased RDW in clinically depressed adolescents.

Methods: Data from depressed adolescent female patients (n = 93) and healthy controls (HC) (n = 43) aged 12-17 years from the AtR!Sk-bio cohort study were retrospectively analysed. We compared RDW between groups and tested whether there was an association between RDW and depression severity and global (psychiatric) symptom severity. We also examined the influence of age on RDW.

Results: There was no significant difference between depressed patients and healthy controls and no association between RDW and depression severity. However, higher RDW values were associated with greater global symptom severity. Regardless of group, there was a positive association between RDW and age.

Conclusions: RDW appears to be unfit as an aid for clinical diagnosis of depression in adolescents, but may be useful in assessing global psychiatric symptom burden.