Search

Objective: Inflamatory processes play an important role in the etiology of psychiatric disorders. The aim of this study was to evaluate inflammatory complete blood count (CBC) parameters in substance use disorder (SUD). Methods: The study included 90 patients with SUD and 90 healthy controls (HC). The Student t-test was used to compare CBC parameters between the groups. The Kruskal – Wallis test was used to compare the data on the basis of substance types. Results: Leukocyte, lymphocyte, and monocyte levels were higher in SUD group than HC. Leukocyte and neutrophil levels of patients with opioid use disorder (OUD) were higher than HC. Platelet levels and neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, and systemic immune inflammation index values were higher in patients with OUD than in patients with non-opioid substance use disorder (nOUD). Moreover, lymphocyte and monocyte levels were higher in patients with nOUD than in HC. Monocyte levels were increased in patients with cannabinoid use disorder compared to HC. Conclusion: The results suggested that inflammatory CBC parameters play an important role in the etiology of SUD according to type of substance. However, there is not enough data for supporting the clinical use of these parameters.. [ABSTRACT FROM AUTHOR]

Introduction: Bipolar disorder (BD), a mood disorder with recurrent affective episodes and a strong genetic basis is frequently associated with significant comorbidities, both physical and psychiatric, yet its neurobiology remains unclear. Recent evidence underscores oxidative stress as a pivotal factor linking BD to its comorbidities, prompting an investigation into whether this is a sign of a genetic vulnerability or a consequence of the disease. In this study, we systematically reviewed oxidative stress studies conducted on individuals at risk for BD. We performed a meta-analysis on studies examining oxidative DNA damage in these individuals. Methods: The literature was searched across the databases PubMed, Web of Science, Scopus, Ovid MEDLINE, and Cochrane to locate studies of oxidative stress markers in relatives of patients with BD compared with healthy controls (from 1946 to March 2024). Studies were considered for inclusion based on the following criteria: (i) involvement of first- or second-degree relatives of individuals diagnosed with BD, (ii) presence of a healthy control group, (iii) reporting of oxidative stress parameters for relatives, including mean and standard deviation or median and interquartile range (25–75%) values, and (iv) publication in the English language. Studies comparing the levels of 8-hydroxy-2′-deoxyguanosine (8-OH-dG) or its tautomer 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxo-dG) in individuals at risk for BD with healthy controls were evaluated using a meta-analysis with the random-effects method. The risk of bias was evaluated using the Risk of Bias in Non-Randomized Studies of Exposure (ROBINS-E) tool. Results: Eleven studies were included in the systematic review and four studies for the meta-analysis. The meta-analysis included 543 individuals (first-degree relatives of individuals with BD = 238, control = 305). 8-OH-dG levels were found to be increased in first-degree relatives of individuals with BD compared to healthy controls (random effects: Hedges's g = 0.53, 95% CI = 0.36–0.71, p < 0.001). Findings of oxidative stress markers other than oxidative DNA damage in relatives of individuals with BD are limited and scarce. Conclusion: In this meta-analysis, which consists of a limited number of studies, oxidative DNA damage seems to be a trait marker for BD. This finding could be associated with increased comorbidity and a higher risk of premature aging in individuals at risk for BD. However, further studies with larger sample sizes and longitudinal designs are warranted to confirm findings. Clarifying the changes in these markers from individuals at risk for the disorder throughout the course of the illness would help bridge the gap in understanding the role of oxidative pathways in the risk of BD. [ABSTRACT FROM AUTHOR]

Aims & Background: Bipolar disorder (BD) has been linked to both epigenetic modifications and mitochondrial dysfunction. Recent research has revealed associations between epigenetic alterations of mitochondrial DNA and mitochondrial dysfunction. Long non-coding RNAs (lncRNAs) play pivotal roles as regulators of gene expression and are involved in the crosstalk between mitochondrial DNA and mitochondrial functioning. This study aimed to compare the expression levels of two mitochondrial-encoded lncRNAs among individuals with BD, their unaffected siblings, and healthy controls. Method: Thirty euthymic medicated individuals with BD (BD), 30 unaffected siblings of individuals with BD (Sib), and 30 healthy controls (HC) provided blood samples after confirmation of diagnoses through SCID-5 interviews. RNA was extracted from peripheral blood mononuclear cells, and the expression levels of lncRNAs (LIPCAR and 7S RNA) and a housekeeping gene (GAPDH) were analyzed using RT-qPCR and calculated using the 2-ΔΔCT formula. Quade's nonparametric univariate analyses of covariance (ANCOVA) models were applied for comparison of lncRNAs, adjusted for age, sex, body mass index, and smoking status. Results & Discussion: Both the expressions of 7S RNA and LIPCAR in the BD group were significantly downregulated compared to the Sib group and HCs. Between Sib and HC, the expression levels of 7S were not different, but the Sib group showed lower expression levels of LIPCAR than HCs. Conclusion: Our findings reveal significant alterations of mitochondrial DNA-encoded lncRNAs in individuals with BD and their healthy siblings. These findings may implicate the roles of mitochondrial DNA epigenetics in the pathogenesis of mitochondrial dysfunction in BD. [ABSTRACT FROM AUTHOR]

Copyright of Archives of Neuropsychiatry / Nöropsikiyatri Arşivi is the property of Turkish Association of Neuropsychiatry and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: Bipolar disorder (BD) and attention deficit hyperactivity disorder (ADHD) often co-occur in adult population. Both conditions present various neurocognitive and behavioral problems. We aimed to examine neurocognitive functions in adult patients with comorbid BD and ADHD (BD+ADHD) in comparison to patients with only BD, only ADHD and healthy controls (HCs). Method: An extensive cognitive battery which evaluates verbal learning and memory, visual memory, processing speed, attention, executive functions, working memory and verbal fluency, was used to assess neurocognitive functions respectively in adult (age 18-65 years) patients with BD (n=37), ADHD (n=43), BD+ADHD (n=20) in comparison to HCs (n=51). The Multivariate Analysis of Covariance models, where age, level of education and total BIS-11 scores were included as covariates, were used for comparing neurocognitive scores among groups. Results: Both BD and BD+ADHD groups showed significantly poorer performance than HCs in processing speed, attention, executive functions, and verbal fluency domains. The BD group had additional significant deficits in executive functions, verbal learning and memory domains. There were no significant differences between BD and BD+ADHD groups with regards to verbal learning and memory, visual memory, processing speed, attention, executive functions, working memory and verbal fluency domains. Patients with only ADHD showed significantly poorer performance than HCs in verbal fluency domain. Conclusions: Our results show similarities in the neurocognitive functions of adults with BD and BD+ADHD across a wide range of cognitive domains. The findings point to the need for further exploration of diverging and converging neurodevelopmental trajectories of BD and ADHD. [ABSTRACT FROM AUTHOR]

Copyright of Turk Psikiyatri Dergisi is the property of Turk Psikiyatri Dergisi and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Tardive dyskinesia is defined as involuntary athetoid or choreiform movements that develop due to the use of neuroleptic drugs for at least a few months. Tongue, lower face, jaw, upper and lower extremities are the most affected parts of the body in tardive dyskinesia. Quality of life is negatively affected because of the low remission rates. Besides tardive dyskinesia, involuntary movements may appear after discontinuation, change or a reduction in the dose of antipsychotic medications, which is called withdrawal-emergent dyskinesia (WED). Unlike tardive dyskinesia, the involuntary movements involve mainly the neck, trunk, and limbs and regress in shorter period of time in WED. A consensus has not yet been reached for the treatment of WED. Restarting the previous antipsychotic agent with slow titration or switching to an atypical antipsychotic with low affinity for dopamine D2 receptors are among the primary options for treatment. As WED is one of the predictors of tardive dyskinesia development, early detection and treatment is believed to have positive effect on the quality of life. In this report, the case of a patient followed up for bipolar disorder type I (BD-I) and started on clozapine for WED after discontinuation of haloperidol on account of adverse effects is discussed. It is necessary for clinicians to consider these types of complications when discontinuing or changing treatment. Further research is needed in order to reach a common approach for the treatment of WED.