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Background: Impulsive aggression represents a frequent characteristic of pediatric bipolar disorder (PBD). Cortical alterations associated with impulsive aggression and its multiple facets have not been investigated yet in youth with bipolar disorder. Aim: To investigate the relationship between cortical thickness and facets of impulsive aggression in youth with PBD. Materials and Methods: Twenty-three youth with PBD and 23 healthy controls (HC) were administered the aggression questionnaire (AQ) and underwent 3T magnetic resonance imaging scan. Cortical thickness was assessed with FreeSurfer. Canonical correlation analyses were used to investigate the relationship between AQ total and subscale scores and cortical thickness in youth with PBD. Results: Youth with PBD had increased scores in the subscales of AQ-anger and AQ-hostility and cortical thinning in in areas belonging to the affective network (AN), frontoparietal network (FPN) and cingulo-opercular network (CON), i.e., right rostral anterior cingulate, right caudal anterior cingulate, right lateral orbitofrontal, right medial orbitofrontal, left and right inferior parietal, left posterior cingulate, left and right supramarginal left lingual cortices. Greater thickness in these networks positively correlated with the AQ-hostility subscale and negatively correlated with AQ-anger subscale. Conclusions: The opposite patterns observed between areas belonging to AN, FPN, CON, and the two facets of IA, namely anger and hostility, corroborate clinical findings supporting the different nature of these two constructs., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Simonetti, Kurian, Saxena, Verrico, Restaino, Di Nicola, Soares, Sani and Saxena.)

The aims of this article are to discuss the rationale, design, and procedures of the Greater Houston Area Bipolar Registry (HBR), which aims at contributing to the effort involved in the investigation of neurobiological mechanisms underlying bipolar disorder (BD) as well as to identify clinical and neurobiological markers able to predict BD clinical course. The article will also briefly discuss examples of other initiatives that have made fundamental contributions to the field. This will be a longitudinal study with participants aged 6-17 at the time of enrollment. Participants will be required to meet diagnostic criteria for BD, or to be offspring of a parent with BD. We will also enroll healthy controls. Besides clinical information, which includes neurocognitive performance, participants will be asked to provide blood and saliva samples as well as to perform neuroimaging exams at baseline and follow-ups. Several studies point to the existence of genetic, inflammatory, and brain imaging alterations between individuals at higher genetic risk for BD compared with healthy controls. Longitudinal designs have shown high conversion rates to BD among high-risk offspring, with attempts to identify clinical predictors of disease onset, as well as clarifying the burden associated with environmental stressors. The HBR will help in the worldwide effort investigating the clinical course and neurobiological mechanisms of affected and high-risk children and adolescents with BD., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Diaz, Cuellar, Vinson, Suchting, Durkin, Fernandes, Scaini, Kazimi, Zunta-Soares, Quevedo, Sanches and Soares.)

Introduction: Post-Traumatic Stress Disorder (PTSD) is often associated with impairments in emotional and cognitive domains. Contrarily to the emotional sphere, neural basis underpinnings to cognitive impairments are still not well known., Methods: We performed a bibliographic search on PUBMED of all the studies investigating the cognitive impairments in PTSD individuals. We considered only studies that applied cognitive tasks using a functional Magnetic Resonance Imaging technique. The inclusion criteria were met by nine studies., Results: Overall, PTSD individuals reported significant impairments in the dorsolateral prefrontal cortex, anterior cingulate cortex, inferior frontal gyrus, insula, inferior temporal cortex, supplement motor area, and Default Mode Network (DMN). Moreover, abnormal activity was reported in subcortical structures (e.g. hippocampus, amygdala, thalamus) and in the cerebellum., Limitations: Cognitive functioning was assessed using different cognitive tasks. Potential confounding factors such as age, sex, symptoms intensity, and comorbidities might have influenced the results., Conclusion: So far, the evidence reported that PTSD is characterized by cognitive impairments in several domains, such as attention, memory and autonomic arousal, which may be due to selective dysfunctions in brain regions that are part of cortical networks, the limbic system and DMN. However, further studies are needed in order to better assess the role of cognitive impairments in PTSD and to develop more targeted therapeutic approaches., (Copyright © 2020 Dossi, Delvecchio, Prunas, Soares and Brambilla.)

Bipolar disorder (BD) is a prevalent mood disorder characterized by alternating episodes of depression and mania, often accompanied by varying degrees of cognitive impairment. Cognitive impairments often serve as indicators of a bleak prognosis or the likelihood of progressing to dementia. Additionally, some studies suggest that individuals diagnosed with BD may undergo a decline in hippocampal volume. However, the potential for reversibility of these changes, particularly in adolescents, remains unclear. We present an intriguing case involving an 18-year-old male student who experiences concurrent occurrences of both BD and mild cognitive impairment (MCI), accompanied by a subtle reduction in hippocampal volume. Initially, the individual exhibited impaired general cognitive function, as indicated by an IQ score of 80 on the Standard Raven's Progressive Matrices test, and demonstrated slightly reduced bilateral hippocampal volume compared to the normative reference, as determined through quantitative structural magnetic resonance imaging (qsMRI). The deposition profiles of amyloid beta (Aβ) peptide in the brain were not identified with 18F-AV45 PET/MRI. Following six months of combined psychopharmacological treatment and cognitive behavioral therapy, the individual's psychopathological symptoms improved significantly, leading to a restoration of his IQ score to 116 and normalization of hippocampal volume. This case suggests that the hippocampal volume reduction and cognitive impairment seen in some adolescents with BD may demonstrate greater plasticity compared to neurodegenerative conditions such as Alzheimer's disease (AD). These findings highlight the potential importance of early intervention in young BD patients with cognitive impairments. [ABSTRACT FROM AUTHOR]

In this review, it is evaluated the progress in the application of stem cell therapy to ameliorate the symptoms of bipolar disorder, major depression, schizophrenia, and autism. These disorders are highly prevalent in clinical medicine and are responsible for high levels of psychosocial disability among patients. All of them share common biomedical features, such as complex and variable genetic substrates, significant susceptibility to environmental changes, and insufficient knowledge of their pathogenesis. In addition, the responsiveness of patients to pharmacological treatment is heterogeneous, and in some cases, no treatment is available. Therefore, the development of stem cell-based regenerative medicine and its possible combination with emerging therapeutic approaches that promote neural plasticity are expected to advance neuropsychiatry in the next few decades. [ABSTRACT FROM AUTHOR]

The article discusses the relationship between urban living and borderline personality disorder (BPD) through neuroplasticity, highlighting the impact of the physical environment on the development and treatment of BPD. It emphasizes the adverse effects of urban environments on brain regions associated with BPD, such as the amygdala, hippocampus, and cortex, leading to maladaptive neuroplasticity outcomes. The article calls for collaborative efforts between therapists, public health policymakers, urban planners, architects, and interior designers to prevent triggering BPD and improve treatment outcomes through environmental interventions. The importance of addressing the physical environment in BPD care pathways is underscored, with recommendations for incorporating environmental factors into treatment strategies. [Extracted from the article]

Background: Previous evidence suggests that immune-inflammatory dysfunction plays an important role in metabolic disorder (MD) of patients with schizophrenia, yet studies on sex differences in the association between both are limited. The current study aimed to investigate sex differences in the association between MD and inflammatory cytokines in Han Chinese patients with chronic schizophrenia (CS). Methods: This multicentre cross-sectional study was conducted in one general hospital and two psychiatric hospitals in Anhui Province, China. General information, metabolic parameters and inflammatory cytokine indicators were collected from all participants, and the severity of their psychiatric symptoms was assessed using the Positive and Negative Syndrome Scale (PANSS). Results: A total of 324 patients completed the assessment and were included in this study. The patients with MD had higher age and duration of illness, and lower chlorpromazine equivalents and negative symptom score than those without MD. Binary logistic regression showed that MD was significantly associated with a higher IL-1β level in male patients, while this association was not significant in females. Further multiple linear regression revealed that IL-1β level was negatively correlated with polypharmacy only in male patients. Conclusion: Sex differences in the association between MD and IL-1β level are significant in patients with CS, and only in male patients is there a negative correlation between MD and IL-1β level. Sex-specific prevention and intervention strategies may contribute to reducing MD in patients with CS. [ABSTRACT FROM AUTHOR]

Background: Depression is a complex mental disease whose incidence increases every year; 300 million people worldwide currently suffer from it. Women are more likely to suffer from depression, twice the rate as men. It is one of the few illnesses that can lead to suicide, which makes it very dangerous – currently, 700,000 people die from suicide and it is the 4th most common cause of death in people aged 15-29. The treatment strategies for depression is a big challenge for physicians, pharmacists, scientists and classic remedies cause many side effects. Therefore, natural phytotherapy with herbs can prove to be a good solution. Phytotherapy is a popular treatment method used for centuries in Chinese medicine or Ayurveda. Materials and methods: The study conducted a comprehensive database search PubMed, ClinicalKey and MedNar covered the years 2015 - 2024 to provide the most up-to-date data. 13 randomized controlled trials and 1 meta – analysis were included in the systematic review. Results: Many plants show anti-inflammatory, antioxidant and cognitive enhancing effects, which are particularly important in depression. In the treatment of depression, plants such as Crocus sativus L. stigma , Lavandula angustifolia, Hypericum perforatum L. and Curcuma longa L. have proven to be effective. They show good effectiveness in human studies and alleviate the symptoms of depression. Herbal products can support classical pharmacotherapy, but this requires further research. Non-commercial clinical trials in the future should provide answers to research questions: at what stage of treatment of patients with MDD will the use of phytochemicals be most appropriate in terms of therapy efficacy and safety for the patient. Conclusions: Crocus sativus L. stigma , Lavandula angustifolia, Hypericum perforatum L. and Curcuma longa L. in modern medicine can help improve the well-being of patients with depression. The use of herbs as an intervention was associated with a decrease in the concentration of proinflammatory cytokines and an overall improvement in the mood of patients. Further research should be undertaken into combining both therapies in order to improve patients' quality of life and reduce treatment costs. [ABSTRACT FROM AUTHOR]

Introduction: The number of insular gyri is elevated in patients with schizophrenia. Thus, it has potential as a marker of early neurodevelopmental abnormalities. However, currently it remains unclear whether patients with other neuropsychiatric disorders, such as affective disorders, also have this gross brain anatomical feature. Materials and methods: The macroscopic features of the insular cortex in 26 patients with bipolar disorder (BD), 56 with major depressive disorder (MDD), and control subjects for each clinical group (24 for BD and 33 for MDD) were assessed using magnetic resonance imaging. Results: The number of short insular gyri was higher in BD patients than in matched controls bilaterally with well-developed accessory and middle short gyri. Furthermore, the left middle short gyrus was more developed in MDD patients than in matched controls, and was weakly associated with the severity of depressive symptoms. Discussion: The present results indicate that changes in the gross morphology of the insular cortex in BD and MDD is a potential vulnerability factor associated with their neurodevelopmental pathologies, and may also contribute to the severity of symptoms in MDD. [ABSTRACT FROM AUTHOR]

Introduction: Schizophrenia (SZ) and bipolar disorder (BD) share common clinical features, symptoms, and neurocognitive deficits, which results in common misdiagnosis. Recently, it has been suggested that alterations within brain networks associated with perceptual organization yield potential to distinguish SZ and BD individuals. The aim of our study was to evaluate whether functional connectivity (FC) of the dorsal attention network (DAN) may differentiate both conditions Methods: The study involved 90 participants: 30 remitted SZ patients, 30 euthymic BD patients, and 30 healthy controls (HC). Resting state functional magnetic resonance imaging was used to compare the groups in terms of the FC within the core nodes of the DAN involving frontal eye fields (FEF) and intraparietal sulcus (IPS) Results: BD patients presented weaker inter-hemispheric FC between right and left FEF than HC. While SZ did not differ from HC in terms of inter-FEF connectivity, they presented increased inter- and intra-hemispheric FC between FEF and IPS. When compared with BD, SZ patients showed increased FC between right FEF and other nodes of the network (bilateral IPS and left FEF) Conclusion: We have shown that altered resting state FC within DAN differentiates BD, SZ, and HC groups. Divergent pattern of FC within DAN, consisting of hypoconnectivity in BD and hyperconnectivity in SZ, might yield a candidate biomarker for differential diagnosis between both conditions. More highly powered studies are needed to confirm these possibilities. [ABSTRACT FROM AUTHOR]

Background: Antipsychotic medications offer limited long-term benefit to about 30% of patients with schizophrenia. We aimed to explore the individual-specific imaging markers to predict 1-year treatment response of schizophrenia. Methods: Structural morphology and functional topological features related to treatment response were identified using an individualized parcellation analysis in conjunction with machine learning (ML). We performed dimensionality reductions using the Pearson correlation coefficient and three feature selection analyses and classifications using 10 ML classifiers. The results were assessed through a 5-fold cross-validation (training and validation cohorts, n = 51) and validated using the external test cohort (n = 17). Results: ML algorithms based on individual-specific brain network proved more effective than those based on group-level brain network in predicting outcomes. The most predictive features based on individual-specific parcellation involved the GMV of the default network and the degree of the control, limbic, and default networks. The AUCs for the training, validation, and test cohorts were 0.947, 0.939, and 0.883, respectively. Additionally, the prediction performance of the models constructed by the different feature selection methods and classifiers showed no significant differences. Conclusion: Our study highlighted the potential of individual-specific network parcellation in treatment resistant schizophrenia prediction and underscored the crucial role of feature attributes in predictive model accuracy. [ABSTRACT FROM AUTHOR]

Introduction: Major Depression (MD) is a common mental disorder. In East Asian ancestry, the association, causality, and shared genetic basis between bloodbased biomarkers and MD remain unclear. Methods: We investigated the relationships between blood-based biomarkers and MD through a cross-sectional study and Mendelian randomization (MR) analysis. Cross-trait analysis and enrichment analyses were used to highlight the shared genetic determinants and biological pathways. We conducted summary data-based MR to identify shared genes, which were then validated using a transcriptome dataset from drug-naïve patients with MD. Results: In the cross-sectional study, C-Reactive Protein showed the significantly positive correlation with depressive symptoms, while hematocrit, hemoglobin, and uric acid exhibited significantly negative correlations. In MR analysis, basophil count (BASO) and low-density lipoprotein cholesterol (LDLc) had a significant causal effect on MD. The enrichment analysis indicated a significant role of inflammatory cytokines and oxidative stress. The shared genes MFN2, FAM55C, GCC2, and SCAPER were validated, with MFN2 identified as a pleiotropic gene involved in MD, BASO, and LDLc. Discussion: This study highlighted that BASO and LDLc have a causal effect on MD in East Asian ancestry. The pathological mechanisms of MD are related not only to inflammatory cytokines and oxidative stress but also to down regulation of MFN2 expression and mitochondrial dysfunction. [ABSTRACT FROM AUTHOR]

Bipolar disorder is a chronic disorder characterized by fluctuations in mood state and energy and recurrent episodes of mania/hypomania and depression. Bipolar disorder may be regarded as a neuro-progressive disorder in which repeated mood episodes may lead to cognitive decline and dementia development. In the current review, we employed genome-wide association studies to comprehensively investigate the genetic variants associated with bipolar disorder and dementia. Thirty-nine published manuscripts were identified: 20 on bipolar disorder and 19 on dementia. The results showed that the genes CACNA1C, GABBR2, SCN2A, CTSH, MSRA, and SH3PXD2A were overlapping between patients with bipolar disorder and dementia. In conclusion, the genes CACNA1C, GABBR2, SCN2A, CTSH, MSRA, and SH3PXD2A may be associated with the neuroprogression of bipolar disorder to dementia. Further genetic studies are needed to comprehensively clarify the role of genes in cognitive decline and the development of dementia in patients with bipolar disorder. [ABSTRACT FROM AUTHOR]

Introduction: Symptoms during the onset of major depressive disorder [MDD] and bipolar disorder type II [BD-II] are similar. The difference of hippocampus subregion could be a biological marker to distinguish MDD from BD-II. Methods: We recruited 61 drug-naïve patients with a first-episode MDD and BD-II episode and 30 healthy controls (HC) to participate in amagnetic resonance imaging [MRI] study. We built a general linear model (one-way analysis of covariance) with 22 hippocampal subfields and two total hippocampal volumes as dependent variables, and the diagnosis of MDD, BD-II, and HC as independent variables. We performed pair-wise comparisons of hippocampal subfield volumes between MDD and HC, BD-II and MDD, BD-II and HC with post hoc for primary analysis. Results: Weidentifiedthree regions that differed significantly in sizebetweenpatients and controls. The left hippocampal fissure, the hippocampal-amygdaloid transition area (HATA), and the right subiculum bodywere all significantly larger in patients with MDD compared with the HC. In the onset of first-episode of MDD, the hippocampal volume increased significantly, especially on the left side comparing toHC. However, we found differences between MDD and BD-II were not statistically significant. The volume of the left HATA and right subiculum body in BD-II was larger. Conclusions: The sample size of this study is relatively small, as it is a crosssectional comparative study. In both MDD and BD-II groups, the volume of more left subregions appeared to increase. The left subregions were severely injured in the development of depressive disorder. [ABSTRACT FROM AUTHOR]

Background: Research on depression showed that dysregulations in tryptophan (TRP), kynurenine (KYN), and its KYN pathway metabolites are key aspects in the development and maintenance of depressive symptoms. In our previous reports, we described sex-specific changes in TRP breakdown as well as changes in KYN and KYN/TRP in association with treatment response and inflammatory and metabolic parameters. However, results of treatment effects on KYN pathway metabolites as well as how pathway changes are related to treatment response remain sparse. Objective: We investigated potential changes of KYN and KYN pathway metabolites in association with therapeutic response of individuals with depression during a six-week multimodal psychiatric rehabilitation program. Methods: 87 participants were divided into treatment responders and nonresponders (48 responders, 39 non-responders; 38 male, 49 female; Mage = 51.09; SDage = 7.70) using scores of psychological questionnaires. KYN pathwaymetabolites serum concentrations as well as their ratios were collected using high performance liquid chromatography. Changes over time (time of admission (t1) vs. time of discharge (t2)) were calculated using repeated measure analyses of (co)variance. Results: Non-responders exhibited higher levels of 3-Hydroxyanthralinic acid (3-HAA), nicotinic acid (NA), and 3-HAA/KYN, independently of measurement time. NA levels decreased, while 3-HAA levels increased over time in both groups, independently of treatment response. 3-HK/KYN levels decreased, while KYN levels increased in non-responders, but not in responders over time. Discussion: The results indicate that some compounds of the KYN pathway metabolites can be altered through multimodal long-term interventions in association with treatment response. Especially the pathway degrading KYN further down to 3-HAA and 3-HK/KYNmight be decisive for treatment response in depression. [ABSTRACT FROM AUTHOR]

Background: With similarities in heritability, neurobiology and symptomatology, the question has been raised whether schizophrenia and bipolar disorder are truly distinctive disorders or belong to a continuum. This narrative review summarizes common and distinctive findings from genetics, neuroimaging, cognition and clinical course that may help to solve this ethiopathogenetic puzzle. Methods: The authors conducted a literature search for papers listed in PubMed and Google Scholar, using the search terms "schizophrenia" and "bipolar disorder" combined with different terms such as "genes", "neuroimaging studies", "phenomenology differences", "cognition", "epidemiology". Articles were considered for inclusion if they were written in English or Spanish, published as full articles, if they compared subjects with schizophrenia and bipolar disorder, or subjects with either disorder with healthy controls, addressing differences between groups. Results: Several findings support the hypothesis that schizophrenia and bipolar disorder are discrete disorders, yet some overlapping of findings exists. The evidence for heritability of both SZ and BD is obvious, as well as the environmental impact on individual manifestations of both disorders. Neuroimaging studies support subtle differences between disorders, it appears to be rather a pattern of irregularities than an unequivocally unique finding distinguishing schizophrenia from bipolar disorder. The cognitive profile displays differences between disorders in certain domains, such as premorbid intellectual functioning and executive functions. Finally, the timing and trajectory of cognitive impairment in both disorders also differs. Conclusion: The question whether SZ and BD belong to a continuum or are separate disorders remains a challenge for further research. Currently, our research tools may be not precise enough to carve out distinctive, unique and undisputable differences between SZ and BD, but current evidence favors separate disorders. Given that differences are subtle, a way to overcome diagnostic uncertainties in the future could be the application of artificial intelligence based on BigData. Limitations: Despite the detailed search, this article is not a full and complete review of all available studies on the topic. The search and selection of papers was also limited to articles in English and Spanish. Selection of papers and conclusions may be biased by the personal view and clinical experience of the authors. [ABSTRACT FROM AUTHOR]

Introduction: Patients with alcohol use disorder (AUD) often experience repeated withdrawal. Impulsivity is the most relevant factor influencing successful withdrawal. Brain-derived neurotrophic factor (BNDF) and fibroblast growth factor 21 (FGF21) are associated with impulsivity. Previous studies on the differential effects of BDNF or FGF21 on impulsivity have focused on single-gene effects and have inconsistent results. We aim to investigate the effects of BDNF rs6265 and FGF21 rs11665896, individually and together, on impulsivity during alcohol withdrawal in patients with AUD. Methods: We recruited 482 adult Han Chinese males with AUD and assessed their impulsivity using the Barratt Impulsivity Scale. Genomic DNA was extracted and genotyped from peripheral blood samples. Statistical analysis was conducted on the data. Results: The T-test and 2 × 2 analysis of variance were used to investigate the effects of the genes on impulsivity. There was a significant BDNF × FGF21 interaction on no-planning impulsiveness (F = 9.15, p = 0.003, η2p= 0.03). Simple main effects analyses and planned comparisons showed that BDNF rs6265 A allele × FGF21 rs11665896 T allele was associated with higher no-planning impulsiveness. Finally, hierarchical regression analyses revealed that only the interaction of BDNF and FGF21 accounted for a significant portion of the variance in no-planning impulsiveness. Conclusion and significance: The combination of BDNF rs6265 A allele and FGF21 rs11665896 T allele may increase impulsivity and discourage alcohol withdrawal. Our study provides a possible genetic explanation for the effects of associated impulsivity in patients with AUD from the perspective of gene-gene interactions. [ABSTRACT FROM AUTHOR]

Objective: Accumulating evidence has indicated that neurodevelopmental defects may underlie the pathophysiology of bipolar disorder (BD). Insulin-like growth factors (IGFs) are a family of neurotrophic factors that are essential for the survival and development of neurons. The present study aims to investigate whether IGF-2 signaling is implicated in the pathophysiological processes of BD. Method: 50 healthy controls and 78 patients with BD, including 23 patients who diagnosed acute depressive episode and 55 patients who diagnosed acute manic episode, were recruited in this study. The 17-item Hamilton Depression Rating Scale (HAMD-17) and the Young Mania Rating Scale (YMRS) were used to assess the severity of the depressive and manic symptoms, respectively. The serum IGF2 level was determined by an enzyme-linked immunosorbent assay (ELISA). The Kolmogorov-Smirnov and Mann-Whitney U tests were used for between-group comparisons and spearman analysis was used to analyze correlations. Results: Patients with BD had lower serum IGF-2 levels (66.08 ± 21.22 ng/ml) when compared to healthy controls (88.72 ± 31.55 ng/ml). BD patients were divided into manic episode and depressive episode subgroups. We found that serum IGF-2 levels were reduced in both the mania and depression subgroups (mania: 67.19 ± 21.52 ng/ml, depression: 63.43 ± 20.67 ng/ml; P < 0.001), while no significant difference was observed between two groups (P > 0.05). Spearman correlation analyses revealed that the levels of serum IGF-2 were negatively correlated with the YMRS scores in BD patients (r = -0.522, P < 0.001). Furthermore, IGF-2 was found to be an independent contributor to the severity of symptoms in patients with manic episodes (B = -0.610, t = -5.299, P < 0.001). Conclusion: Lower serum IGF-2 levels were found in BD patients and correlated with the severity of the manic symptoms in these patients during manic episodes. These results suggest that reduced IGF-2 levels might be involved in the pathophysiology of BD, and serum IGF-2 could be a peripheral biomarker for the evaluation of the severity of manic symptoms in BD patients. [ABSTRACT FROM AUTHOR]

Introduction: Research has indicated that individuals diagnosed with bipolar disorder (BD) might experience alterations in their olfaction or levels of serum tumor necrosis factor-α (TNF-α), but no studies have investigated olfactory function and serum TNF-α in BD patients simultaneously. Moreover, there is a lack of existing research that compares the longitudinal olfactory function between individuals with manic and euthymic BD I. Methods: Patients with manic BD I (BDM, n=44) and healthy controls (HCs, n=32) were evaluated symptoms (measured via the Young Manic Rating Scale, YRMS), social function (measured via the Global Assessment Function, GAF), serum TNFa, and olfactory function (via the Sniffin’ Sticks test) including olfactory sensitivity (OS) and olfactory identification (OI). The BDM patients were followed up to the remission period and re-evaluated again. We compared OS, OI and serum TNF-α in manic and euthymic patients with BD I and HCs. We examined the correlation between olfactory function and symptoms, social function, and serum TNF-α in patients with BD I. Results: The BDM patients exhibited significantly lower OS and OI compared to the HCs (Z = −2.235, P = 0.025; t = −6.005, P < 0.001), while a positive correlation was observed between OS and GAF score (r = 0.313, P = 0.039). The OS in the BD I remission group (n=25) exhibited significantly superior performance compared to the BDM group (t = −4.056, P < 0.001), and the same as that in the HCs (P = 0.503). The change in OS showed a positive correlation with the decrease in YMRS score (r = 0.445, P = 0.026), and a negative correlation with the course of disease (r = -0.594, P = 0.002). The TNF-α in BD I patients was significantly lower compared to HCs (P < 0.001), and not significantly correlated with olfactory function (all P > 0.05). Conclusion: The findings suggest that OS and OI are impaired in BDM patients, and the impaired OS in those patients can be recovered in the remission stage. OI may serve as a potential characteristic marker of BD. OS might be useful as an index for BDM treatment efficacy and prognosis. [ABSTRACT FROM AUTHOR]

Introduction: Individuals with depression who do not respond to two or more courses of serotonergic antidepressants tend to have greater deficits in reward processing and greater internalizing symptoms, yet there is no validated self-report method to determine the likelihood of treatment resistance based on these symptom dimensions. Methods: This online case-control study leverages machine learning techniques to identify differences in self-reported anhedonia and internalizing symptom profiles of antidepressant non-responders compared to responders and healthy controls, as an initial proof-of-concept for relating these indicators to medication responsiveness. Random forest classifiers were used to identify a subset from a set of 24 reward predictors that distinguished among serotonergic medication resistant, non-resistant, and non-depressed individuals recruited online (N = 393). Feature selection was implemented to refine model prediction and improve interpretability. Results: Accuracies for full predictor models ranged from .54 to .71, while feature selected models retained 3-5 predictors and generated accuracies of .42 to .70. Several models performed significantly above chance. Sensitivity for non- responders was greatest after feature selection when compared to only responders, reaching .82 with 3 predictors. The predictors retained from feature selection were then explored using factor analysis at the item level and cluster analysis of the full data to determine empirically driven data structures. Discussion: Non-responders displayed 3 distinct symptom profiles along internalizing dimensions of anxiety, anhedonia, motivation, and cognitive function. Results should be replicated in a prospective cohort sample for predictive validity; however, this study demonstrates validity for using a limited anhedonia and internalizing self-report instrument for distinguishing between antidepressant resistant and responsive depression profiles. [ABSTRACT FROM AUTHOR]

Objective: Although the adverse effects of obesity in schizophrenia are documented, there is limited research exists on the implications for untreated initial schizophrenia. Our investigation aimed to explore the connections between BMI and cognitive function in first-episode drug-naïve (FEDN)schizophrenia. Methods: We enrolled 143 FEDN schizophrenia patients, and collected data on their body mass index, fasting blood glucose and lipid levels. Cognitive function was measured with the MATRICS Consensus Cognitive Battery (MCCB). Using correlation and regression analysis to assess the relationship between BMI and cognitive performance. Results: The prevalence rate of overweight plus obesity in FEDN schizophrenia patients was 33.57%. Patients with FEDN schizophrenia exhibited extensive cognitive impairment, and those who were overweight/obesity demonstrated more severe impairments in working memory and visual learning when compared to normal/under weight counterparts. Correlation analysis indicated a negative association between working memory and BMI and TG, as well as a link between visual learning and BMI and LDL-C. Multiple linear regression analysis revealed that a higher BMI predicted a decrease in working memory in FEDN schizophrenia patients. Conclusion: Our results indicate that the rate of overweight plus obesity is high in FEDN schizophrenia patients, and there is an association between BMI and cognitive function in schizophrenia, particularly in relation to working memory. [ABSTRACT FROM AUTHOR]

Borderline personality disorder (BPD), a complex and severe psychiatric disorder, has become a topic of considerable interest to current researchers due to its high incidence and severity of consequences. There is a lack of a bibliometric analysis to visualize the history and developmental trends of researches in BPD. We retrieved 7919 relevant publications on the Web of Science platform and analyzed them using software CiteSpace (6.2.R4). The results showed that there has been an overall upward trend in research interest in BPD over the past two decades. Current research trends in BPD include neuroimaging, biological mechanisms, and cognitive, behavioral, and pathological studies. Recent trends have been identified as “prevention and early intervention”, “non-pharmacological treatment” and “pathogenesis”. The results are like a reference program that will help determine future research directions and priorities. [ABSTRACT FROM AUTHOR]

Background: Cognitive reserve (CR) is a complex concept that includes premorbid IQ, years of education, and exposure to neuropsychological stimuli through work and leisure. Previous studies have suggested that CR has a positive impact on several aspects of bipolar disorder. Synthesizing the evidence to date is an important work in providing directions for future studies. The objectives of this systematic review to summary impact of CR on onsetting, relapsing bipolar episodes, buffering cognitive dysfunctions, and maintaining quality of life (QOL) in bipolar disorder. Methods: Two researchers independently reviewed selected paper from three database as PubMed, PsychINFO, and Web of Science. The search keywords were "bipolar disorder" and "cognitive reserve." The selected studies were classified as the levels of evidence according to the criteria of the Oxford Center for Evidence-Based Medicine. The results of the selected studies were summarized according to the objectives. Results: Thrity six studies were included in this review. People with high CR may have fewer bipolar episodes and alleviate cognitive impairments and dysfunction. CR may keep the functional level in patients with bipolar disorder. Conclusion: The results of this systematic review suggest that CR may be involved in preventing relapse of bipolar episodes and may alleviate cognitive dysfunction. However, effect on prevention of onset-risk and relapse of bipolar episodes need further investigation in prospective studies. [ABSTRACT FROM AUTHOR]

Introduction: Subanesthetic ketamine is a rapidly acting antidepressant that has also been found to improve neurocognitive performance in adult patients with treatment resistant depression (TRD). Provisional evidence suggests that ketamine may induce change in hippocampal volume and that larger pre-treatment volumes might be related to positive clinical outcomes. Here, we examine the effects of serial ketamine treatment on hippocampal subfield volumes and relationships between pre-treatment subfield volumes and changes in depressive symptoms and neurocognitive performance. Methods: Patients with TRD (N = 66; 31M/35F; age = 39.5 ± 11.1 years) received four ketamine infusions (0.5 mg/kg) over 2 weeks. Structural MRI scans, the National Institutes of Health Toolbox (NIHT) Cognition Battery, and Hamilton Depression Rating Scale (HDRS) were collected at baseline, 24 h after the first and fourth ketamine infusion, and 5 weeks post-treatment. The same data was collected for 32 age and sex matched healthy controls (HC; 17M/15F; age = 35.03 ± 12.2 years) at one timepoint. Subfield (CA1/CA3/CA4/subiculum/molecular layer/GC-ML-DG) volumes corrected for whole hippocampal volume were compared across time, between treatment remitters/non-remitters, and patients and HCs using linear regression models. Relationships between pre-treatment subfield volumes and clinical and cognitive outcomes were also tested. All analyses included Bonferroni correction. Results: Patients had smaller pre-treatment left CA4 (p = 0.004) and GC.ML. DG (p = 0.004) volumes compared to HC, but subfield volumes remained stable following ketamine treatment (all p > 0.05). Pre-treatment or change in hippocampal subfield volumes over time showed no variation by remission status nor correlated with depressive symptoms (p > 0.05). Pre-treatment left CA4 was negatively correlated with improved processing speed after single (p = 0.0003) and serial ketamine infusion (p = 0.005). Left GC.ML.DG also negatively correlated with improved processing speed after single infusion (p = 0.001). Right pretreatment CA3 positively correlated with changes in list sorting working memory at follow-up (p = 0.0007). Discussion: These results provide new evidence to suggest that hippocampal subfield volumes at baseline may present a biomarker for neurocognitive improvement following ketamine treatment in TRD. In contrast, pre-treatment subfield volumes and changes in subfield volumes showed negligible relationships with ketamine-related improvements in depressive symptoms. [ABSTRACT FROM AUTHOR]

Background: White matter hyperintensities are lesions of presumed vascular origin associated with Cerebral small vessel disease. WMH are common findings that and are associated with increased risk of cognitive impairment and dementia. A higher prevalence of WMH has been also reported in patients with bipolar disorder (BD), although the evidence is conflicting. Objective: To compare the prevalence of WMH in adults with BD, with the prevalence found in healthy controls. Methods: We searched the Embase, Medline/PubMed, and references cited in articles retrieved on May 20, 2023. We included case-control studies that compared the prevalence of WMH in adult BD patients with the prevalence of WMH in healthy controls, using T2-weighted magnetic resonance imaging. We performed a meta-analysis using a random-effects method based on the inverse-variance approach. Findings: We included 22 case-control studies reporting data of 1313 people. The overall rate of WMH was 46.5% in BD patients and 28% in controls (pooled Odds Ratio 2.89, 95% CI 1.76; 4.75). We found a moderate heterogeneity across studies (I2 = 0.49). Publication bias was not significant. Interpretation: We found evidence that BD patients have a higher burden of WMH than healthy controls. Main limitations were impossibility of analyzing gender differences and bipolar type, moderate heterogeneity between studies, non-representative samples, lack of control for major confounders and search in two electronic databases. [ABSTRACT FROM AUTHOR]

Objective: The treatment of bipolar disorder (BD) remains challenging. The study evaluated the impact of the hypothalamic-pituitary-adrenal (HPA) axis/hypothalamic-pituitary-thyroid (HPT) axis and glucose metabolism on the clinical outcomes in patients with bipolar depression (BD-D) and manic bipolar (BD-M) disorders. Methods: The research design involved a longitudinal prospective study. A total of 500 BD patients aged between 18 and 65 years treated in 15 hospitals located in Western China were enrolled in the study. The Young Mania Rating Scale (YMRS) and Montgomery and Asberg Depression Rating Scale (MADRS) were used to assess the BD symptoms. An effective treatment response was defined as a reduction in the symptom score of more than 25% after 12 weeks of treatment. The score of symptoms was correlated with the homeostatic model assessment of insulin resistance (HOMA-IR) index, the HPA axis hormone levels (adrenocorticotropic hormone (ACTH) and cortisol), and the HPT axis hormone levels (thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), free triiodothyronine (fT3), and free thyroxine (fT4)). Results: In the BD-M group, the YMRS was positively correlated with baseline T4 (r = 0.349, p = 0.010) and fT4 (r = 0.335, p = 0.013) and negatively correlated with fasting insulin (r = -0.289, p = 0.013). The pre-treatment HOMA-IR was significantly correlated with adverse course (p = 0.045, OR = 0.728). In the BD-D group, the baseline MADRS was significantly positively correlated with baseline fT3 (r = 0.223, p = 0.032) and fT4 (r = 0.315, p = 0.002), while baseline T3 (p = 0.032, OR = 5.071) was significantly positively related to treatment response. Conclusion: The HPT axis and glucose metabolism were closely associated with clinical outcomes at 12 weeks in both BD-D and BD-M groups. If confirmed in further longitudinal studies, monitoring T3 in BD-D patients and HOMA-IR for BD-M could be used as potential treatment response biomarkers. [ABSTRACT FROM AUTHOR]

Background: Prenatal depressive symptoms (PDS) is a serious public health problem. This study aimed to develop an integrated panel and nomogram to assess at-risk populations by examining the association of PDS with the serum metabolome, multivitamin supplement intake, and clinical blood indicators. Methods: This study comprised 221 pregnant women, categorized into PDS and non-PDS groups based on the Edinburgh postnatal depression scale. The participants were divided into training and test sets according to their enrollment time. We conducted logistic regression analysis to identify risk factors, and employed liquid chromatography/high resolution mass spectrometry-based serum metabolome analysis to identify metabolic biomarkers. Multiple factor analysis was used to combine risk factors, clinical blood indicators and key metabolites, and then a nomogram was developed to estimate the probability of PDS. Results: We identified 36 important differential serum metabolites as PDS biomarkers, mainly involved in amino acid metabolism and lipid metabolism. Multivitamin intake works as a protective factor for PDS. The nomogram model, including multivitamin intake, HDL-C and three key metabolites (histidine, estrone and valylasparagine), exhibited an AUC of 0.855 in the training set and 0.774 in the test set, and the calibration curves showed good agreement, indicating that the model had good stability. Conclusion: Our approach integrates multiple models to identify metabolic biomarkers for PDS, ensuring their robustness. Furthermore, the inclusion of dietary factors and clinical blood indicators allows for a comprehensive characterization of each participant. The analysis culminated in an intuitive nomogram based on multimodal data, displaying potential performance in initial PDS risk assessment. [ABSTRACT FROM AUTHOR]

This review sought to summarize the literature on current practices and forms of psychoeducation in the management of patients with bipolar disorder (BD), including only randomized controlled trials to ensure the best level of evidence. An extensive review of the available literature was conducted using PubMed/MEDLINE, Embase, and PsychInfo databases from inception to April 28th, 2022. The search yielded 381 studies. Seventy articles were included after removing duplicates and applying the inclusion/ exclusion criteria. A best-evidence synthesis was used to identify the key results of each study and summarize the outcomes. Eleven descriptive categories were made. They encompass different forms of psychoeducation compared or combined with other psychosocial interventions, varying in setting (individual or group), with or without family members, structured or unstructured, mediated or not by digital tools (smartphone, internet). Globally, these studies show that psychoeducation is important in the treatment of BD, as it leads to a decrease in relapses, mood episodes, hospitalizations, and improved functioning or quality of life. Some studies also showed the benefits of psychoeducation on the patient's level of knowledge of pharmacological treatment and the disorder or compliance with medication, as well as reduced self-stigma. The limitations of this review are linked to the selection of only RCTs and the reliance on their post-hoc analyses. This review confirms the benefit of psychoeducation and psychosocial interventions on the evolution of BD (in different outcomes, including quality of life, relapse, and rehospitalization rates, for example). More recent interventions, such as mindfulness or online psychoeducation, represent an interesting option but more evidence is needed. [ABSTRACT FROM AUTHOR]

Introduction: Few controlled trials have assessed the benefits of Mindfulness Based Cognitive Therapy (MBCT) on cognitive functions and brain-derived neurotrophic factor (BDNF) in bipolar disorder (BD). This study aims to evaluate the impact of MBCT adjunctive treatment on these variables. Main hypothesis was that MBCT would improve cognitive functioning and BDNF more than Psychoeducation and TAU. Methods: Randomized, multicenter, prospective and single-blinded trial. Included BD outpatients randomly assigned to three treatment arms: MBCT plus treatment as usual (TAU), Psychoeducation plus Tau and TAU. Cognitive functions were assessed with Continuous Performance Test-III, Stroop Test, Trail Making Test, Digit Span and Letter-Number Sequencing from Wechsler Adult Intelligence Scale III, Face Emotion Identification Task and Face Emotion Discrimination Task. BDNF serum level was measured with ELISA. Patients were assessed at baseline, 8 weeks and 6 months. Results: Eighty-four patients were recruited (TAU = 10, Psychoeducation = 34, MBCT = 40). No significant differences between treatment groups were found. MBCT does not achieve better results than Psychoeducation or TAU. Discussion: Being Psychoeducation and TAU efficient interventions, as well as the scarce duration of a more complex intervention, such as MBCT, are suggested as explanatory variables of these results. [ABSTRACT FROM AUTHOR]

Objectives: The identification of molecular biomarkers for bipolar disorder is anticipated to greatly improve the diagnosis and treatment of this disease. The objective of this case--control study is to determine whether the blood thyroid hormone levels in bipolar disorder patients are associated with different types of first onset. Methods: From August 1, 2020 to July 31, 2021 a total of 120 female patients diagnosed with bipolar disorder and hospitalized at Qingdao Mental Health Center were recruited as the case group, including 60 patients with depression as their first onset (depression first-episode group, DF) and 60 with mania/hypomania as their first onset (mania/hypomania first-episode group, M/HF). A group of 60 healthy adult females matching general demographic data, such as race and age, were selected as the control group. Blood samples were taken from both groups to measure serum triiodothyronine (T3), thyroxine (T4), free triiodothyronine (FT3), free thyroxine (FT4), and thyroid stimulating hormone (TSH) concentrations. Results: The duration of current onset in the M/HF group was significantly less than that in the DF group (23.1 ± 20.2 vs. 125.2 ± 41.0 days). About 27% of patients in the M/HF group had thyroid abnormalities, in contrast to 60% in the DF group. The blood T3 and T4 levels in both the M/HF group and the DF group, as well as the TF3 levels in the DF group, were significantly lower as compared to control. The M/HF group had significantly higher T3 and FT3 levels than the DF group. The blood T3 levels were inversely correlated with the Young's Mania Scale score and the Hamilton Depression Scale score in both the M/HF and DF groups. Conclusion: Thyroid dysfunction resulting in reduced levels of blood thyroid levels may be involved in the disease progression of bipolar disorder, and correlated with the clinical symptoms in patients with depression or mania as the first episode. [ABSTRACT FROM AUTHOR]

Depression has long been considered a disease involving immune hyperactivation. The impact of pro-inflammatory cytokines such as TNF-a, IL-1ß, IL-6, and IL-8 on depression has been widely studied. However, the effect of IL-33, another pro-inflammatory cytokine, has been less researched. Currently, research on the correlation between IL-33 and depression risk is inconsistent. In response to these divergent results, we conducted a review and meta-analysis aimed at resolving published research on the correlation between IL-33 and depression risk, and understanding the potential role of IL-33 in the development and treatment of depression. After searching different databases, we analyzed 8 studies. Our meta-analysis showed that IL-33 had a positive correlation with reduced risk of depression. The pooled standard mean differences (SMD) = 0.14, 95% confidence interval (CI): 0.05-0.24. Subgroup analysis results showed that IL-33 and ST2 levels in cerebrospinal fluid and serum is positive correlated with reduced risk of major depressive disorder (MDD) and bipolar disorder (BD). According to the characteristics of the included literature, the results mainly focuses on Caucasian. Furthermore, according to the subgroup analysis of depression-related data sources for disease or treatment, the correlation between IL-33 and depression risk is reflected throughout the entire process of depression development and treatment. Therefore, the change of IL-33 level in serum and cerebrospinal fluid can serve as useful indicators for assessing the risk of depression, and the biomarker provides potential treatment strategies for reducing the burden of the disease. [ABSTRACT FROM AUTHOR]

Background: Deep brain stimulation (DBS) is still an experimental treatment modality for psychiatric disorders including treatment-resistant depression (TRD). There is preliminary evidence that stimulation of brain reward circuit structures including the ventral striatum (VS) may exert an antidepressant effect. The main nucleus of the reward circuit is the nucleus accumbens (NAc). The NAc is a major structure of VS that plays a critical role in reward-seeking behavior, motivation, and addiction. Aims: This study aimed to review the current studies including randomized clinical trials, open-label trials, and case reports of NAc/VS and VC DBS for TRD in humans. Method: The literature was reviewed using a medical database--Medical Literature, Analysis, and Retrieval System Online (MEDLINE) on NAc/VS or VC DBS in TRD. The identified studies were assessed based on the patient's characteristics, clinical outcomes, and adverse events related to DBS as well as the stereotactic technique used to guide the implantation of DBS electrodes. The inclusion and exclusion criteria of DBS for TRD were presented and discussed. Results: The searched literature revealed one case report, three open-label studies (OLS), one multicenter open-label study (mOLS), and two randomized clinical trials (RCTs). There were three additional studies reporting the clinical outcomes in the long term in TRD patients included in the two mentioned RCTs. The total number of patients with TRD treated by NAc/VS or VC is estimated to be 85 individuals worldwide. The response rate to DBS defined as a 50% reduction of postoperative Montgomery-Asberg Depression Rating Scale (MADRS) scores was achieved in 39.8% of the operated patients (range, 23-53%). The remission defined as MADRS scores of < 10 was found in 17.8% after DBS (range, 0-40%). The mean follow-up was 19.7 months (range 3.7-24 months). Conclusion: The current results of NAc/VS and VC DBS are still limited by a relatively small number of patients treated worldwide. Nevertheless, the results suggest that NAc/VS and VC can be regarded as promising and efficacious targets for DBS, taking into account the response and remission rates among TRD patients with no other treatment option. The adverse events of NAc/VS and VC DBS are reversible due to the adjustment of stimulation parameters. The most common adverse events were hypomanic/manic states, suicidal thoughts/attempts, and suicides. Patients with TRD after NAc/VS and VC DBS should be strictly followed to prevent or diminish these stimulation-induced adverse events. [ABSTRACT FROM AUTHOR]

Introduction: Subanesthetic ketamine is a rapidly acting antidepressant that has also been found to improve neurocognitive performance in adult patients with treatment resistant depression (TRD). Provisional evidence suggests that ketamine may induce change in hippocampal volume and that larger pre-treatment volumes might be related to positive clinical outcomes. Here, we examine the effects of serial ketamine treatment on hippocampal subfield volumes and relationships between pre-treatment subfield volumes and changes in depressive symptoms and neurocognitive performance. Methods: Patients with TRD (N = 66; 31M/35F; age = 39.5 ± 11.1 years) received four ketamine infusions (0.5 mg/kg) over 2 weeks. Structural MRI scans, the National Institutes of Health Toolbox (NIHT) Cognition Battery, and Hamilton Depression Rating Scale (HDRS) were collected at baseline, 24 h after the first and fourth ketamine infusion, and 5 weeks post-treatment. The same data was collected for 32 age and sex matched healthy controls (HC; 17M/15F; age = 35.03 ± 12.2 years) at one timepoint. Subfield (CA1/CA3/CA4/subiculum/molecular layer/GC-ML-DG) volumes corrected for whole hippocampal volume were compared across time, between treatment remitters/non-remitters, and patients and HCs using linear regression models. Relationships between pre-treatment subfield volumes and clinical and cognitive outcomes were also tested. All analyses included Bonferroni correction. Results: Patients had smaller pre-treatment left CA4 (p = 0.004) and GC.ML. DG (p = 0.004) volumes compared to HC, but subfield volumes remained stable following ketamine treatment (all p > 0.05). Pre-treatment or change in hippocampal subfield volumes over time showed no variation by remission status nor correlated with depressive symptoms (p > 0.05). Pre-treatment left CA4 was negatively correlated with improved processing speed after single (p = 0.0003) and serial ketamine infusion (p = 0.005). Left GC.ML.DG also negatively correlated with improved processing speed after single infusion (p = 0.001). Right pretreatment CA3 positively correlated with changes in list sorting working memory at follow-up (p = 0.0007). Discussion: These results provide new evidence to suggest that hippocampal subfield volumes at baseline may present a biomarker for neurocognitive improvement following ketamine treatment in TRD. In contrast, pre-treatment subfield volumes and changes in subfield volumes showed negligible relationships with ketamine-related improvements in depressive symptoms. [ABSTRACT FROM AUTHOR]

Type I Bipolar disorder (BD-I) is a neuropsychiatric disorder characterized by manic or mixed-featured episodes, impaired cognitive functioning, and persistent work and social functioning impairment. This study aimed to investigate withinsubject; (i) differences in brain perfusion using Single-photon emission computed tomography (SPECT) between manic and euthymic states in BD-I patients; (ii) explore potential associations between altered brain perfusion and cognitive status; and (iii) examine the relationship between cerebral perfusion and mania symptom ratings. Seventeen adult patients diagnosed with BD-I in a manic episode were recruited, and clinical assessments, cognitive tests, and brain perfusion studies were conducted at baseline (mania state) and a follow-up visit 6 months later. The results showed cognitive impairment during the manic episode, which persisted during the euthymic state at follow-up. However, no significant changes in brain perfusion were observed between the manic and euthymic states. During mania, trends toward decreased perfusion in the left cerebellum and right superior parietal lobule were noted. Additionally, trends indicated a higher perfusion imbalance in the left superior and middle frontal gyrus during mania and the right superior and middle frontal gyrus during euthymia. No significant correlations existed between brain perfusion, mania symptom ratings, and cognitive performance, indicating that symptomatology might represent more than neural hemodynamics. These findings suggest that cognitive impairment may persist in BD-I patients and highlight the need for therapeutic interventions targeting cognitive deficits. More extensive studies with extended follow-up periods are warranted further to investigate brain perfusion and cognitive functioning in BD-I patients. [ABSTRACT FROM AUTHOR]

Introduction: This study describes the differences and similarities in mental health, substance use, and substance use treatment outcomes between people presenting for SUD treatment who identified as transgender and those who identified as cisgender men or women. Methods: We compared 64 individuals who self-identified as transgender and presented for SUD treatment to samples of cisgender men and women (separately) matched based on propensity scores which were created based on sociodemographic factors known to influence both the nature of substance use and patterns of treatment engagement including age, education, race, stable housing, and employment status. Comparisons were made using χ² tests and t-tests in over 150 variables collected at treatment intake regarding physical and mental health, substance use patterns, events that led to treatment, reasons for seeking treatment, and treatment outcomes. Results: The transgender sample endorsed six of the seven suicide-related items more often than at least one of the cisgender-matched samples. Furthermore, the transgender sample remained in treatment significantly longer (M = 32.3, SD = 22.2) than the cisgender male sample (M = 19.5, SD = 26.1, t = 2.17, p = 0.03). Discussion: This study is a first step into understanding gender minority population experiences during SUD treatment. While there was no significant difference between the cisgender and transgender samples on most variables, there was an elevated prevalence of suicidal ideation and behaviors in the transgender sample, which warrants further investigation. [ABSTRACT FROM AUTHOR]

Introduction: The dysregulation of psychophysiological responses to mental stressors is a common issue addressed in individuals with psychiatric conditions, while brain circuit abnormalities are often associated with psychiatric conditions and their manifestations. However, to our knowledge, there is no systematic overview that would comprehensively synthesize the literature on psychophysiological responses during laboratory-induced psychosocial stressor and neural correlates in people with mental disorders. Thus, we aimed to systematically review the existing research on psychophysiological response during laboratory-induced stress and its relationship with neural correlates as measured by magnetic resonance imaging techniques in mental disorders. Methods: The systematic search was performed on PubMed/Medline, EBSCOhost/PsycArticles, Web of Science, and The Cochrane Library databases during November 2021 following the PRISMA guidelines. Risk of bias was evaluated by employing the checklists for cross-sectional and case-control studies from Joanna Briggs Institute (JBI) Reviewers Manual. Results: Out of 353 de-duplicated publications identified, six studies were included in this review. These studies were identified as representing two research themes: (1) brain anatomy and psychophysiological response to mental stress in individuals with mental disorders, and (2) brain activity and psychophysiological response to mental stress in individuals with mental disorders. Conclusions: Overall, the evidence from studies exploring the interplay between stress psychophysiology and neural correlates in mental disorders is limited and heterogeneous. Further studies are warranted to better understand the mechanisms of how psychophysiological stress markers interplay with neural correlates in manifestation and progression of psychiatric illnesses. [ABSTRACT FROM AUTHOR]

Background: Bipolar disorder (BD) is a chronic and disabling affective disorder with significant morbidity and mortality. Despite the high rate of psychiatric and physical health comorbidity, little is known about the complex interrelationships between clinical features of bipolar illness and comorbid conditions. The present study sought to examine, quantify and characterize the cross-sectional associations of psychiatric and physical comorbidities with selected demographic and clinical characteristics of adults with BD. Methods: A nationwide multicenter cross-sectional observational epidemiological study conducted from October 2015 to March 2017 in Slovakia. Results: Out of 179 study participants [median age 49 years (interquartile range IQR 38-58); 57.5% females], 22.4% were free of comorbidity, 42.5% had both psychiatric and physical comorbidities, 53.6% at least one psychiatric comorbidity, and 66.5% at least one physical comorbidity. The most prevalent were the essential hypertension (33.5%), various psychoactive substance-related disorders (21.2%), specific personality disorders (14.6%), obesity (14.5%), and disorders of lipoprotein metabolism (14%). The presence of an at least one physical comorbidity, atypical symptoms of BD, and unemployed status were each associated with an at least one psychiatric comorbidity independent of sex, early onset of BD (age of onset <35 years), BD duration and pattern of BD illness progression (p < 0.001). The presence of various psychoactive substance-related disorders, BD duration, atypical symptoms of BD, unemployed status, pension, female sex, and not using antipsychotics were each associated with an at least one physical comorbidity independent of the pattern of BD illness progression (p < 0.001). In several other multiple regression models, the use of antipsychotics (in particular, olanzapine) was associated with a decreased probability of the essential hypertension and predicted the clinical phenotype of comorbidity-free BD (p < 0.05). Conclusion: This cross-national study has reported novel estimates and clinical correlates related to both the comorbidity-free phenotype and the factors associated with psychiatric and physical comorbidities in adults with BD in Slovakia. The findings provide new insights into understanding of the clinical presentation of BD that can inform clinical practice and further research to continue to investigate potential mechanisms of BD adverse outcomes and disease complications onset. [ABSTRACT FROM AUTHOR]

Background: Reversible splenial lesion syndrome (RESLES) is a rare neurological condition characterized by temporary abnormalities in the splenium of the corpus callosum, which has been reported in mental disorders. Previous studies on bipolar disorder (BD) primarily focused on aspects such as brain structure and function, neurochemical changes, and genetics. However, there have been no studies reporting the occurrence of this syndrome during hypomanic episodes and its disappearance during the remission phase in bipolar disorder type 2 (BD-II). Case presentation: We present a case report of a 30 years-old female patient with BD-II who exhibited symptoms of RESLES during a hypomanic episode. The patient, with a 12 years psychiatric history, has experienced recurrent depressive episodes initially, with the first hypomanic episode occurring 8 years ago. During this period, this patient made several visits to the outpatient clinic to have her medications adjusted due to repeated suicide attempts. This time, she was admitted to our hospital with a second hypomanic episode due to drug withdrawal during pregnancy. The RESLES was observed on her brain magnetic resonance image, and it was alleviated after treatment with lithium carbonate and quetiapine until achieving remission. Conclusion: We present the first report of identifying RESLES in BD-II with hypomanic episodes, which subsequently disappears during the remission phase. Our case report highlights a potential association between BD and RESLES, emphasizing the need for future studies to explore the underlying mechanisms connecting these two conditions in greater depth. [ABSTRACT FROM AUTHOR]

Purposes: This study aimed to analyze the predictive ability of the complete blood count and derived inflammatory indicators for BD patients with different states to identify potential biomarkers. Methods: We collected the data of BD in-patients from January 2021 to March 2023. The complete blood count and derived inflammatory indicators were computed by univariate analysis, logistic regression analysis, and receiver operating characteristic (ROC) curve analysis. Results: In terms of BD patients, the levels of MON (p<0.0001), hs-CRP (p = 0.018), and NLR (p = 0.002) were independent risk factors in logistic regression analysis, as well as the cut-off values were 0.405 109/L, 2.600 mg/L, and 2.321, respectively. Regarding BD-M patients, the levels of MON (p<0.0001), hs-CRP (p = 0.012), and NLR (p = 0.002) were predictors in logistic regression analysis, and the cutoff values were, respectively, 0.505 109/L, 2.600 mg/L, and 2.620. Additionally, the levels of NLR (p = 0.006) and MHR (p<0.0001) were important indicators for BD-D and the cut-off values were 1.735 and 0.487, respectively. Furthermore, our findings showed that the level of MON (p = 0.001) was related to BD-mixed and the cut-off value was 0.340 109/L. Notably, MON+hs-CRP + NLR, MON+hs- CRP + NLR, and NLR + MHR had the highest diagnostic accuracy to predict BD, BD-M, and BD-D patients, respectively. Conclusion: Our findings showed that distinct inflammatory indicators were closely associated with BD and its different states. Additionally, we also identified their cut-off values and optimal combined predictive indicators in different states of BD, helping us improve diagnostic accuracy and better assess them to manage early targeted interventions. [ABSTRACT FROM AUTHOR]

Background: Social interaction is a fundamental human need. Social isolation (SI) can have negative effects on both emotional and cognitive function. However, it is currently unclear how age and the duration of SI affect emotion and recognition function. In addition, there is no specific treatment for the effects of SI. Methods: The adolescence or adult mice were individually housed in cages for 1, 6 or 12 months and for 2 months to estabolish SI mouse model. We investigated the effects of SI on behavior in mice at different ages and under distinct durations of SI, and we explored the possible underlying mechanisms. Then we performed deep brain stimulation (DBS) to evaluate its influences on SI induced behavioral abnormalities. Results: We found that social recognition was affected in the short term, while social preference was damaged by extremely long periods of SI. In addition to affecting social memory, SI also affects emotion, short-term spatial ability and learning willingness in mice. Myelin was decreased significantly in the medial prefrontal cortex (mPFC) and dorsal hippocampus of socially isolated mice. Cellular activity in response to social stimulation in both areas was impaired by social isolation. By stimulating the mPFC using DBS, we found that DBS alleviated cellular activation disorders in the mPFC after long-term SI and improved social preference in mice. Conclusion: Our results suggest that the therapeutic potential of stimulating the mPFC with DBS in individuals with social preference deficits caused by long-term social isolation, as well as the effects of DBS on the cellular activity and density of OPCs. [ABSTRACT FROM AUTHOR]

Introduction: The U.S. suicide mortality rate has steadily increased during the past two decades, particularly among military veterans; however, the epigenetic basis of suicidal thoughts and behaviors (STB) remains largely unknown. Methods: To address this issue, we conducted an epigenome-wide association study of DNA methylation (DNAm) of peripheral blood samples obtained from 2,712 U.S. military veterans. Results: Three DNAm probes were significantly associated with suicide attempts, surpassing the multiple testing threshold (FDR q-value <0.05), including cg13301722 on chromosome 7, which lies between the genes SLC4A2 and CDK5; cg04724646 in PDE3A; and cg04999352 in RARRES3. cg13301722 was also found to be differentially methylated in the cerebral cortex of suicide decedents in a publicly-available dataset (p = 0.03). Trait enrichment analysis revealed that the CpG sites most strongly associated with STB in the present sample were also associated with smoking, alcohol consumption, maternal smoking, and maternal alcohol consumption, whereas pathway enrichment analysis revealed significant associations with circadian rhythm, adherens junction, insulin secretion, and RAP-1 signaling, each of which was recently associated with suicide attempts in a large, independent genome-wide association study of suicide attempts of veterans. Discussion: Taken together, the present findings suggest that SLC4A2, CDK5, PDE3A, and RARRES3 may play a role in STB. CDK5, a member of the cyclindependent kinase family that is highly expressed in the brain and essential for learning and memory, appears to be a particularly promising candidate worthy of future study; however, additional work is still needed to replicate these finding in independent samples. [ABSTRACT FROM AUTHOR]

Background: Since being recognized as an important drug-induced clinical entity during the 1960s, tardive dyskinesia (TD) has generated an extensive body of research seeking to understand its clinical characteristics, epidemiology, pathophysiology and management. Modern scientometric approaches allow interactive visualization of large bodies of literature to identify trends and hotspots within knowledge domains. This study thus aimed to provide a comprehensive scientometric review of the TD literature. Methods: Web of Science was searched for articles, reviews, editorials and letters with the term "tardive dyskinesia" in the title, abstract, or keywords through 12/31/2021. A total of 5,228 publications and 182,052 citations were included. Annual research output, prominent research areas, authors, affiliations and countries were summarized. VOSViewer and CiteSpace were used for bibliometric mapping and co-citation analysis. Structural and temporal metrics were used to identify key publications in the network. Results: TD-related publications peaked in the 1990s, gradually declined after 2004, and showed a further small increase after 2015. The most prolific authors were Kane JM, Lieberman JA, and Jeste DV overall (1968-2021), and Zhang XY, Correll CU and Remington G in the last decade (2012-2021). The most prolific journal was the Journal of Clinical Psychiatry overall, and the Journal of Psychopharmacology in the last decade. Knowledge clusters in the 1960-1970s dealt with clinical and pharmacological characterization of TD. In the 1980s, epidemiology, clinical TD assessment, cognitive dysfunction and animal models predominated. During the 1990s, research diverged into pathophysiological studies, especially oxidative stress, and clinical trials on atypical antipsychotics, with a focus on clozapine and bipolar disorder. In the 1990-2000s, pharmacogenetics emerged. More recent clusters include serotonergic receptors, dopamine-supersensitivity psychosis, primary motor abnormalities of schizophrenia, epidemiology/meta-analyses, and advances in TD treatment, particularly vesicular monoamine transporter-2 inhibitors since 2017. Conclusion: This scientometric review visualized the evolution of scientific knowledge on TD over more than five decades. These findings will be useful for researchers to find relevant literature when writing scientific articles, choosing appropriate journals, finding collaborators or mentors for research, and to understand the historical developments and emerging trends in TD research. [ABSTRACT FROM AUTHOR]

Psychiatric comorbidity is the norm in the assessment and treatment of eating disorders (EDs), and traumatic events and lifetime PTSD are often major drivers of these challenging complexities. Given that trauma, PTSD, and psychiatric comorbidity significantly influence ED outcomes, it is imperative that these problems be appropriately addressed in ED practice guidelines. The presence of associated psychiatric comorbidity is noted in some but not all sets of existing guidelines, but they mostly do little to address the problem other than referring to independent guidelines for other disorders. This disconnect perpetuates a "silo effect," in which each set of guidelines do not address the complexity of the other comorbidities. Although there are several published practice guidelines for the treatment of EDs, and likewise, there are several published practice guidelines for the treatment of PTSD, none of them specifically address ED+PTSD. The result is a lack of integration between ED and PTSD treatment providers, which often leads to fragmented, incomplete, uncoordinated and ineffective care of severely ill patients with ED+PTSD. This situation can inadvertently promote chronicity and multimorbidity and may be particularly relevant for patients treated in higher levels of care, where prevalence rates of concurrent PTSD reach as high as 50% with many more having subthreshold PTSD. Although there has been some progress in the recognition and treatment of ED+PTSD, recommendations for treating this common comorbidity remain undeveloped, particularly when there are other cooccurring psychiatric disorders, such as mood, anxiety, dissociative, substance use, impulse control, obsessive-compulsive, attention-deficit hyperactivity, and personality disorders, all of which may also be trauma-related. In this commentary, guidelines for assessing and treating patients with ED+PTSD and related comorbidity are critically reviewed. An integrated set of principles used in treatment planning of PTSD and trauma-related disorders is recommended in the context of intensive ED therapy. These principles and strategies are borrowed from several relevant evidence-based approaches. Evidence suggests that continuing with traditional single-disorder focused, sequential treatment models that do not prioritize integrated, trauma-focused treatment approaches are short-sighted and often inadvertently perpetuate this dangerous multimorbidity. Future ED practice guidelines would do well to address concurrent illness in more depth. [ABSTRACT FROM AUTHOR]

Objective: Brain-derived neurotrophic factor (BDNF) has not been validated as a diagnostic marker for Alzheimer's disease (AD). To provide a different perspective, this study aimed to evaluate the relationship between serumlevels of mature BDNF (mBDNF) and precursor BDNF (proBDNF) in AD and to investigate whether serum BDNF levels or the ratio of mBDNF levels to proBDNF levels (M/P) could be a valuable biomarker for determining the risk of AD in elderly individuals. Method: A total of 126 subjects who met the inclusion criteria were assigned to either the AD group (n = 62) or the healthy control group (HC, n = 64) in this cross-sectional observationl study. Serum levels of mBDNF and proBDNF were measured using enzyme immunoassay kits. We analyzed the Mini-Mental State Examination (MMSE) scores from the two groups and examined the associations between AD and BDNF metabolism. Results: The serum concentration of proBDNF was significantly higher in ADs (4140.937 pg/ml) than in HCs (2606.943 pg/ml; p < 0.01). The MMSE significantly correlated with proBDNF (p < 0.01, r = -0.686) and M/P (p < 0.01, r = 0.595) in all subjects. To determine the risk for AD, the area under the receiver operating characteristic curve was calculated, which was 0.896 (95% confidence interval 0.844-0.949) for proBDNF and 0.901 (95% 0.850-0.953) for proBDNF and M/P combined. Conclusion: We observed a correlation between low serum proBDNF levels and higher MMSE scores in AD. The most effective diagnostic strategy was the combination of proBDNF andM/P, whereasmBDNF levels performed poorly when we evaluated the predictive model. [ABSTRACT FROM AUTHOR]

Background: Major depressive disorder (MDD) is a prevalent health problem with complex pathophysiology that is not clearly understood. Prior work has implicated the hippocampus in MDD, but how hippocampal subfields influence or are affected by MDD requires further characterization with high-resolution data. This will help ascertain the accuracy and reproducibility of previous subfield findings in depression as well as correlate subfield volumes with MDD symptom scores. The objective of this study was to assess volumetric differences in hippocampal subfields between MDD patients globally and healthy controls (HC) as well as between a subset of treatment-resistant depression (TRD) patients and HC using automatic segmentation of hippocampal subfields (ASHS) software and ultra-high field MRI. Methods: Thirty-five MDD patients and 28 HC underwent imaging using 7-Tesla MRI. ASHS software was applied to the imaging data to perform automated hippocampal segmentation and provide volumetrics for analysis. An exploratory analysis was also performed on associations between symptom scores for diagnostic testing and hippocampal subfield volumes. Results: Compared to HC, MDD and TRD patients showed reduced right-hemisphere CA2/3 subfield volume (p = 0.01, η2 = 0.31 and p = 0.3, η2 = 0.44, respectively). Additionally, negative associations were found between subfield volumes and life-stressor checklist scores, including left CA1 (p = 0.041, f2 = 0.419), left CA4/DG (p = 0.010, f2 = 0.584), right subiculum total (p = 0.038, f2 = 0.354), left hippocampus total (p = 0.015, f2 = 0.134), and right hippocampus total (p = 0.034, f2 = 0.110). Caution should be exercised in interpreting these results due to the small sample size and low power. Conclusion: Determining biomarkers for MDD and TRD pathophysiology through segmentation on high-resolution MRI data and understanding the effects of stress on these regions can enable better assessment of biological response to treatment selection and may elucidate the underlying mechanisms of depression. [ABSTRACT FROM AUTHOR]

Background: Treatment-resistant depression remains one of the main concerns of modern psychiatry. Novel methods such as Transcranial Magnetic Stimulation (including deep and theta burst protocols, iTBS) and Deep Brain Stimulation (DBS) can be considered as alternative treatment options. Case presentation: Twenty-nine-year-old Caucasian female, single, higher-educated was treated with major depressive disorder initially with standard pharmaco- and psychotherapy. Due to diagnosed treatment resistance additional therapeutic approaches were introduced sequentially: Electroconvulsive therapy (efficient only 4 months) and Transcranial Magnetic Stimulation (intermittent Theta Burst Stimulation, iTBS improved just insomnia). Finally the patient was enrolled to the Deep Brain Stimulation (DBS) study with the medial forebrain bundle target. After 20 months of active DBS a reduction of over 80% of depressive symptom severity was observed (Montgomery-Asberg and Hamilton Depression Rating Scales), together with an 87% reduction of anxiety symptoms intensity (Hamilton Anxiety Rating Scale) and a 90% increase in social and occupational functioning. Subjective assessment of the patient performed with questionnaires and visual analog scales showed less pronounced improvement in terms of depressive and anxiety symptoms, and high reduction of anhedonia. Some mild, transient side effects of neurostimulation were eliminated with an adjustment in stimulation parameters. Conclusions: The presented clinical case confirms the possibility of achieving remission after the use of MFB DBS in treatment-resistant depression, but postponed formanymonths. Nevertheless, personalization of every combined therapy with DBS is necessary with exploration of individual factors as past traumas and personality traits. More reports on long-term observations in DBS treatment in TRD trials (especially focused on MFB target) are needed. [ABSTRACT FROM AUTHOR]

Psychiatric symptoms frequently predate or complicate neurological disorders, such as neurodegenerative diseases. Symptoms of bipolar spectrum disorders (BSD), like mood, behavioral, and psychotic alterations, are known to occur - individually or as a syndromic cluster - in Parkinson's disease and in the behavioral variant of frontotemporal dementia (FTD). Nonetheless, due to shared pathophysiological mechanisms, or genetic predisposition, several other neurological disorders show significant, yet neglected, clinical and biological overlaps with BSD like neuroinflammation, ion channel dysfunctions, neurotransmission imbalance, or neurodegeneration. BSD pathophysiology is still largely unclear, but large-scale network dysfunctions are known to participate in the onset of mood disorders and psychotic symptoms. Thus, functional alterations can unleash BSD symptoms years before the evidence of an organic disease of the central nervous system. The aim of our narrative review was to illustrate the numerous intersections between BSD and neurological disorders from a clinical-biological point of view and the underlying predisposing factors, to guide future diagnostic and therapeutical research in the field. [ABSTRACT FROM AUTHOR]

Objective: Postpartum depression (PPD) is a serious condition with debilitating consequences for the mother, offspring, and the whole family. The scope of negative outcomes of PPD highlights the need to specify effective diagnostics and treatment which might differ from major depressive disorder (MDD). In order to improve our clinical care, we need to better understand the underlying neuropathological mechanisms of PPD. Therefore, we conducted a systematic review of published neuroimaging studies assessing functional, structural, and metabolic correlates of PPD. Methods: Relevant papers were identified using a search code for Englishwritten studies in the PubMed, Scopus, and Web of Science databases published by March 2022. Included were studies with structural magnetic resonance imaging, functional magnetic resonance imaging, both restingstate and task-related, magnetic resonance spectroscopy, or positron emission tomography. The findings were analyzed to assess signatures in PPD-diagnosed women compared to healthy controls. The review protocol was registered in PROSPERO (CRD42022313794). Results: The total of 3,368 references were initially identified. After the removal of duplicates and non-applicable papers, the search yielded 74 fulltext studies assessed for eligibility. Of them, 26 met the inclusion criteria and their findings were analyzed and synthesized. The results showed consistent functional, structural, and metabolic changes in the default mode network and the salient network in women with PPD. During emotion-related tasks, PPD was associated with changes in the corticolimbic system activity, especially the amygdala. Discussion: This review offers a comprehensive summary of neuroimaging signatures in PPD-diagnosed women. It indicates the brain regions and networks which show functional, structural, and metabolic changes. Our findings offer better understanding of the nature of PPD, which clearly copies some features of MDD, while differs in others. [ABSTRACT FROM AUTHOR]

Objective: Bipolar depression (BD) and major depressive disorder (MDD) are both common affective disorders. The common depression episodes make it difficult to distinguish between them, even for experienced clinicians. Failure to properly diagnose them in a timely manner leads to inappropriate treatment strategies. Therefore, it is important to distinguish between BD and MDD. The aim of this study was to develop and validate a nomogram model that distinguishes BD from MDD based on the characteristics of lymphocyte subsets. Materials and methods: A prospective cross-sectional study was performed. Blood samples were obtained from participants who met the inclusion criteria. The least absolute shrinkage and selection operator (LASSO) regression model was used for factor selection. A differential diagnosis nomogram for BD and MDD was developed using multivariable logistic regression and the area under the curve (AUC) with 95% confidence interval (CI) was calculated, as well as the internal validation using a bootstrap algorithm with 1,000 repetitions. Calibration curve and decision curve analysis (DCA) were used to evaluate the calibration and clinical utility of the nomogram, respectively. Results: A total of 166 participants who were diagnosed with BD (83 cases) or MDD (83 cases), as well as 101 healthy controls (HCs) between June 2018 and January 2022 were enrolled in this study. CD19C B cells, CD3C T cells, CD3--CD16/56C NK cells, and total lymphocyte counts were strong predictors of the diagnosis of BD and MDD and were included in the differential diagnosis nomogram. The AUC of the nomogram and internal validation were 0.922 (95%; CI, 0.879--0.965), and 0.911 (95% CI, 0.838--0.844), respectively. The calibration curve used to discriminate BD from MDD showed optimal agreement between the nomogram and the actual diagnosis. The results of DCA showed that the net clinical benefit was significant. Conclusion: This is an easy-to-use, repeatable, and economical nomogram for differential diagnosis that can help clinicians in the individual diagnosis of BD and MDD patients, reduce the risk of misdiagnosis, facilitate the formulation of appropriate treatment strategies and intervention plans. [ABSTRACT FROM AUTHOR]