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Suicide is a complex and multifaceted public health issue that has been intensively studied to identify its contributing factors. Serotonin, a neurotransmitter essential for affective regulation and mood control, has been linked to suicidal propensity. Understanding the relative contribution of serotonin's genetic versus non-genetic influences is essential for the development of effective preventive measures, given that the etiology of suicide involves both genetic and non-genetic factors. This review seeks to compare the influence of genetic and non-genetic factors on the association between serotonin and suicide risk. Examining serotonin-related gene polymorphisms, with a focus on the serotonin transporter gene, the serotonin receptor 1A, and the serotonin receptor 2A, genetic contributions are investigated. This review emphasizes the complex interplay between genetic and non-genetic contributions to serotonin's role in suicide by synthesizing existing literature. Understanding these complex interactions can provide a comprehensive framework for targeted interventions and individualized methods of suicide prevention and mental health promotion. Future research should incorporate large-scale genetic studies, genetic and non-genetic interaction analyses, and longitudinal designs in order to further elucidate the complex relationship between serotonin and suicide risk. [ABSTRACT FROM AUTHOR]

Background and objectives: The situation caused by the confinement due to the COVID-19 pandemic and the mobility restriction implemented by governments worldwide had a significant impact on people's routines. Stressors are known to increase emotional imbalance, uncertainty, and frustration in the general population. This study explores the factors that predispose to the risk of perceived stress from COVID-19 and determines the underlying mediating mechanisms in the Ecuadorian population. Method: The cross-sectional study an incidental non-probabilistic sample of n = 977 participating student volunteers from the four regions of the Republic of Ecuador (68.6% women and 31.4% men). Data on emotional regulation (ERQ), perceived stress (PSS), active procrastination (APS), diagnosis and symptoms related to COVID-19, social isolation, coexistence, and a sociodemographic questionnaire (biological sex, marital status, and age) were recruited. Statistical analysis was based on a structural equation model. Results: The risk of suffering perceived stress in the COVID-19 pandemic was higher for single women who have lived longer in social isolation, have lived with more people, have poor emotional regulation and high rates of procrastination. This structural model is similar in all Ecuadorian regions χ² = 21.54 (p = 0.760), RMSEA = 0.001 (95%CI, 0.00-0.02), CFI = 0.998; TLI = 0.999; SRMR = 0.020. Discussion: Although our findings are consistent and revealing for the scientific community, the lack of discrimination of the data due to strict isolation measures, taken at different periods by the Ecuadorian government against positive cases of COVID-19, is discussed. The research was applied to the university population, it would be representative to extend the study to schools and colleges. Conclusion: We consider this work as a starting point for the creation of preventive models against perceived stress in the university environment in the event of health emergencies. [ABSTRACT FROM AUTHOR]

Background: Panic disorder and panic attacks are two of the most common problems in psychiatry. A psychoimmunological correlation between allergic diseases and panic disorder has been strongly suggested. Histamine H1 receptor antagonists have been suggested as alternative drugs for the treatment of panic disorder. Chronic spontaneous urticaria (CSU) and panic disorder improved simultaneously with selective serotonin reuptake inhibitor antidepressants. Panic disorder has also been treated with the antihistamine chlorpheniramine. The immunoglobulin/histamine complex is a histamine-fixed immunoglobulin preparation that was reported to be effective in treating CSU. This case report describes the successful treatment of a patient with concomitant panic disorder and CSU for 23 years using immunoglobulin/histamine complex therapy. Case presentation: This report describes a 52-year-old female Korean patient who suffered from CSU with panic disorder for 23 years. Basic allergy tests (blood tests and skin prick tests) were conducted before and after treatment for the evaluation of allergic conditions. A multiple allergosorbent test (MAST) for the detection of allergen-specific IgE levels was also performed. The clinical severity of CSU was evaluated using the urticaria severity score system. Diagnostic interviews systematically assessed the diagnostic criteria outlined by the DSM-V, and the patient was evaluated before, during and after treatment using the Beck Depression Inventory (BDI-2) for depression, the State-Trait Anxiety Inventory (STAI) for anxiety and the Beck Hopelessness Score (BHS) for hopelessness. The patient received 2 ml of Histobulin™ (12 mg human immunoglobulin/0.15 µg histamine complex) once a week by subcutaneous injection for the treatment of CSU. Initial improvement of CSU was achieved after the third injection. After the twenty-seventh injection of Histobulin™, she showed no symptoms or signs and ceased allergic medication use. With the remission of CSU, allergic rhinitis was also completely resolved. The frequency of the common cold was significantly decreased during and after treatment. The medication frequency and development of clinical manifestations of panic disorder changed in parallel with the clinical severity of CSU. Moreover, the patient exhibited no clinical manifestations and ceased medication for panic disorder and sleeping pills for insomnia simultaneously with the remission of CSU. In the psychological evaluation, the BDI, STAI and BHS scores improved accordingly. Conclusions: The immunoglobulin/histamine complex was effective in treating CSU and concomitant panic disorder in this patient and could be effective in treating some types of panic disorder. Considering the mechanisms of action of histamine and the immunoglobulin/histamine complex together with the patient's clinical progress, histamine seemed to be related to panic disorder in this case. The concept of histamine-mediated syndromes, including allergies and psychiatric disorders, shows that a wider disease identity may be needed. Further studies on the immunopathogenesis of panic disorder and the mechanisms of action of the immunoglobulin/histamine complex are necessary. [ABSTRACT FROM AUTHOR]

Background: Food insecurity is prevalent in Canada and may influence mental health, particularly among females. The present study examined the joint effect of female sex and food insecurity on mood disorders. Methods: The study used data from 104,420 adults aged 18 years or older who participated in the 2017/2018 Canadian Community Health Survey (CCHS). Log-binomial models explored the independent and joint associations of female sex and food insecurity with the prevalence of self-reported mood disorder. Prevalence ratios (PRs) and 95% confidence intervals (CIs) were estimated. Relative excess risk due to interaction (RERI), attributable proportion (AP), and synergy index (S) were used to assess the additive interaction of female sex and food insecurity. The complex survey design was taken into consideration. Results: The prevalence of mood disorder was 6.7% for males and 11.4% for females, with an adjusted prevalence ratio being 1.59 (95% CI 1.51, 1.68) for females versus males. Mood disorder was associated with moderate food insecurity (PR 2.06, 95% CI 1.91, 2.23) and severe food insecurity (PR 3.29, 95% CI 3.06, 3.55). There was a significant additive interaction between female sex and food insecurity in association with the prevalence of mood disorders among females aged 18 to 39 years (RERI 1.19, 95% CI 0.27,2.08). Conclusion: Food insecurity was associated with an increased prevalence of mood disorders, especially in younger females. Interventions that facilitate access to food while being cognizant of the socioeconomic vulnerabilities of females may have substantial benefits for the prevention and management of mood disorders. [ABSTRACT FROM AUTHOR]

Obesity is associated with adverse effects on brain health, including an increased risk of neurodegenerative diseases. Changes in cerebral metabolism may underlie or precede structural and functional brain changes. While bariatric surgery is known to be effective in inducing weight loss and improving obesity‐related medical comorbidities, few studies have examined whether it may be able to improve brain metabolism. In the present study, we examined changes in cerebral metabolite concentrations in participants with obesity who underwent bariatric surgery. Thirty‐five patients with obesity (body mass index ≥ 35 kg/m2) were recruited from a bariatric surgery candidate nutrition class. They completed single voxel proton magnetic resonance spectroscopy at baseline (presurgery) and within 1 year postsurgery. Spectra were obtained from a large medial frontal brain region using a PRESS sequence on a 3‐T Siemens Verio scanner. The acquisition parameters were TR = 3000 ms and TE = 37 ms. Tissue‐corrected metabolite concentrations were determined using Osprey. Paired t‐tests were used to examine within‐subject change in metabolite concentrations, and correlations were used to relate these changes to other health‐related outcomes, including weight loss and glycated hemoglobin (HbA1c), a measure of blood sugar levels. Bariatric surgery was associated with a reduction in cerebral choline‐containing compounds (Cho; t [34] = − 3.79, p < 0.001, d = −0.64) and myo‐inositol (mI; t [34] = − 2.81, p < 0.01, d = −0.47) concentrations. There were no significant changes in N‐acetyl‐aspartate, creatine, or glutamate and glutamine concentrations. Reductions in Cho were associated with greater weight loss (r = 0.40, p < 0.05), and reductions in mI were associated with greater reductions in HbA1c (r = 0.44, p < 0.05). In conclusion, participants who underwent bariatric surgery exhibited reductions in cerebral Cho and mI concentrations, which were associated with improvements in weight loss and glycemic control. Given that elevated levels of Cho and mI have been implicated in neuroinflammation, reduction in these metabolites after bariatric surgery may reflect amelioration of obesity‐related neuroinflammatory processes. As such, our results provide evidence that bariatric surgery may improve brain health and metabolism in individuals with obesity. [ABSTRACT FROM AUTHOR]

Introduction: Changes in the DNA methylation of 5-HTTLPR are associated with the pathophysiology of panic disorder (PD). This study was conducted to investigate the association between stressful life events and the level of 5-HTTLPR methylation in patients with PD. We also examined whether these factors were associated with white matter alterations in psychological trauma-related regions. Methods: The participants comprised 232 patients with PD and 93 healthy adults of Korean descent. DNA methylation levels of five cytosine-phosphate-guanine (CpG) sites in the 5-HTTLPR region were analyzed. Voxel-wise statistical analysis of diffusion tensor imaging data was performed within the trauma-related regions. Results: PD patients showed significantly lower levels of the DNA methylation at 5-HTTLPR 5 CpG sites than healthy controls. In patients with PD, the DNA methylation levels at 5-HTTLPR 5 CpG sites showed significant negative association with the parental separation-related psychological distress, and positive correlations with the fractional anisotropy values of the superior longitudinal fasciculus (SLF) which might be related to trait anxiety. Conclusion: Early life stress was significantly associated with DNA methylation levels at 5-HTTLPR related to the decreased white matter integrity in the SLF region in PD. Decreased white matter connectivity in the SLF might be related to trait anxiety and is vital to the pathophysiology of PD. [ABSTRACT FROM AUTHOR]

Major depressive disorder (MDD) etiology is still not completely understood, and many individuals resist the traditional treatments. Chronic exposure to stressful events can contribute to development and progression and be involved in biological changes underlying MDD. Among the biological mechanisms involved, inflammatory changes and oxidative balance are associated with MDD pathophysiology. Quetiapine, a second-generation antipsychotic, induces a better therapeutic response in individuals refractory to traditional treatments. The main objectives of this research were as follows: to evaluate the effect of chronic mild stress (CMS) on depressive-like behaviors, oxidative stress, and inflammation in adult rats; to evaluate the possible antidepressant, antioxidant, and anti-inflammatory effects of quetiapine. The animals were submitted to CMS protocols. At the end of the CMS, the animals were submitted to a chronic treatment for 14 days with the following drugs: quetiapine (20 mg/kg), imipramine (30 mg/kg), and escitalopram (10 mg/kg). At the end of the treatments, the animals were evaluated in the open field tests, anhedonia (splash test), and forced swimming. The animals were euthanized after the behavioral tests, and serum samples were collected. Myeloperoxidase (MPO) activity and interleukin-6 (IL-6) levels were analyzed. CMS induced an increase in depressive-like behaviors, and quetiapine significantly reduced these behaviors. MPO activity and IL-6 levels increased in the serum of animals submitted to CMS. Quetiapine significantly reduced MPO activity and IL-6 levels. These results corroborate other evidence, indicating that chronic stress is a relevant phenomenon in the etiology of depression and suggesting that quetiapine induces an antidepressant effect because it reduces oxidative and inflammatory mechanisms. [ABSTRACT FROM AUTHOR]

Electroconvulsive therapy (ECT) is an important treatment for depression. Although it is known as the most effective acute treatment for severe mood disorders, its therapeutic mechanism is still unclear. With the rapid development of neuroimaging technology, various neuroimaging techniques have been available to explore the alterations of the brain by ECT, such as structural magnetic resonance imaging, functional magnetic resonance imaging, magnetic resonance spectroscopy, positron emission tomography, single photon emission computed tomography, arterial spin labeling, etc. This article reviews studies in neuroimaging on ECT for depression. These findings suggest that the neurobiological mechanism of ECT may regulate the brain functional activity, and neural structural plasticity, as well as balance the brain's neurotransmitters, which finally achieves a therapeutic effect. [ABSTRACT FROM AUTHOR]

The effect of adverse childhood experiences (ACEs) on left ventricular mass (LVM) and left ventricular function remains largely unknown across the lifespan. This study investigated the influence of ACEs on LVM and left ventricular function and whether inflammation influences this relationship. Two hundred forty-eight healthy young adults participated and a final sample of 217 (age, 22.6 ± 0.1 yr; females, 114) had complete data. Echocardiographic assessment of LVM was indexed to height2.7 (LVMHT) and body surface area (LVMBSA). Ejection fraction (EF) and fractional shortening were also assessed. Interleukin-6 (IL-6), C-reactive protein, tumor necrosis factor-a, and matrix metalloproteinase (MMP) 1-3 were measured and ACEs exposures were assessed based on exposure and nonexposure to childhood household dysfunction and maltreatment, and quantity of adversity, (i.e., <4 ACEs and ≥4 ACEs). Individuals who experienced household dysfunction demonstrated lower LVM, LVMHT, and LVMBSA (P < 0.01) and greater IL-6 (P < 0.05) than those who did not experience household dysfunction. Reduced MMP3 was present in individuals who experienced maltreatment (P < 0.05) and ≥4 ACEs (P < 0.01) compared with no maltreatment and <4 ACEs, respectively. After controlling for covariates (i.e., sex, recent life stress, height, body mass index, smoking, physical activity, and inflammation), a significant negative effect of household dysfunction on LVM, LVMHT, and LVMBSA persisted. Likewise, a negative effect on EF independent of covariates was observed in individuals who experienced ≥4 ACEs. As such, alterations in LVM and EF may be perpetuated through a toxic home environment, promoting left ventricular underdevelopment in young adulthood. The effect of which in midlife and beyond requires additional investigation. NEW & NOTEWORTHY This is the first study to investigate the influence of adverse childhood experiences (ACEs) on left ventricular mass (LVM) and function. We identified experiencing any childhood household dysfunction was associated with lower LVM in young adults independent of sex, recent life stress, BMI and height, smoking, physical activity, and inflammation. We speculate an inflection point in LVM occurs in midlife predisposing these individuals toward a hypertrophic profile and elevated risk of heart disease in later life, although this requires longitudinal investigation. [ABSTRACT FROM AUTHOR]

Background: Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a multifaceted condition that affects most body systems. There is currently no known diagnostic biomarker; instead, diagnosis is dependent on application of symptom-based case criteria following exclusion of any other potential medical conditions. While there are some studies that report potential biomarkers for ME/CFS, their efficacy has not been validated. The aim of this systematic review is to collate and appraise literature pertaining to a potential biomarker(s) which may effectively differentiate ME/CFS patients from healthy controls. Methods: This systematic review was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses and Cochrane review guidelines. PubMed, Embase and Scopus were systematically searched for articles containing "biomarker" and "ME/CFS" keywords in the abstract or title and if they included the following criteria: (1) were observational studies published between December 1994 and April 2022; (2) involved adult human participants; (3) full text is available in English (4) original research; (5) diagnosis of ME/CFS patients made according to the Fukuda criteria (1994), Canadian Consensus Criteria (2003), International Consensus Criteria (2011) or Institute of Medicine Criteria (2015); (6) study investigated potential biomarkers of ME/CFS compared to healthy controls. Quality and Bias were assessed using the Joanna Briggs Institute Critical Appraisal Checklist for Case Control Studies. Results: A total of 101 publications were included in this systematic review. Potential biomarkers ranged from genetic/epigenetic (19.8%), immunological (29.7%), metabolomics/mitochondrial/microbiome (14.85%), endovascular/circulatory (17.82%), neurological (7.92%), ion channel (8.91%) and physical dysfunction biomarkers (8.91%). Most of the potential biomarkers reported were blood-based (79.2%). Use of lymphocytes as a model to investigate ME/CFS pathology was prominent among immune-based biomarkers. Most biomarkers had secondary (43.56%) or tertiary (54.47%) selectivity, which is the ability for the biomarker to identify a disease-causing agent, and a moderate (59.40%) to complex (39.60%) ease-of-detection, including the requirement of specialised equipment. Conclusions: All potential ME/CFS biomarkers differed in efficiency, quality, and translatability as a diagnostic marker. Reproducibility of findings between the included publications were limited, however, several studies validated the involvement of immune dysfunction in the pathology of ME/CFS and the use of lymphocytes as a model to investigate the pathomechanism of illness. The heterogeneity shown across many of the included studies highlights the need for multidisciplinary research and uniform protocols in ME/CFS biomarker research. [ABSTRACT FROM AUTHOR]

Introduction: Behavioral-education interventions have the potential to improve quality of life and self-care for patients on hemodialysis (HD) but have not been incorporated into routine clinical practice. The purpose of this pilot study was to determine the feasibility of delivering a simple behavioral-education intervention using cognitive behavioral strategies in patients receiving HD with poor quality of life. Methods: In this mixed methods study, HD patients were randomly assigned to the study intervention (8 behavioral-education sessions delivered over 12 weeks) or a control group of dialysis education alone. Kidney disease quality of life (KDQOL)-36 scores, depressive symptoms and self-care behaviors were measured at weeks 0, 8, and 16. Following study completion, participants, social workers, and physicians provided their perspectives about the intervention via qualitative interviews. Findings: Forty-five participants were randomized. Due, in part, to social worker attrition from the intervention arm, 34 participants (76%) completed at least 1 study session and were included in the analysis. The intervention led to modest, but non-significant, increase in KDQOL-physical component summary scores (+3.1±1.2 points) from week 0 to week 16. There were small, non-significant decreases in interdialytic weight gain and pre-dialysis phosphorus levels in the intervention group. Participants felt that chair-side delivery was practical and efficient, and that content related to the impact of dialysis on daily life was unique and important. Suggestions for adapting the intervention included narrowing its content and its delivery by additional providers that are not necessarily therapy trained. Discussion: In this pilot study, we were able to deliver a simple behavioral-education intervention to improve both quality of life and self-care. Participants had a positive impression of the intervention, but we did not find significant improvements in quality of life or self-care. We will now adapt our intervention by narrowing its content and by using other providers that are focused solely on delivering the intervention. [ABSTRACT FROM AUTHOR]

Background: Chronic morphine usage induces lasting molecular and microcellular adaptations in distinct brain areas, resulting in addiction-related behavioural abnormalities, drug-seeking, and relapse. Nonetheless, the mechanisms of action of the genes responsible for morphine addiction have not been exhaustively studied. Methods: We obtained morphine addiction-related datasets from the Gene Expression Omnibus (GEO) database and screened for Differentially Expressed Genes (DEGs). Weighted Gene Co-expression Network Analysis (WGCNA) functional modularity constructs were analyzed for genes associated with clinical traits. Venn diagrams were filtered for intersecting common DEGs (CDEGs). Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis for functional annotation. Protein–protein interaction network (PPI) and CytoHubba were used to screen for hub genes. Potential treatments for morphine addiction were figured out with the help of an online database. Results: Sixty-five common differential genes linked to morphine addiction were identified, and functional enrichment analysis showed that they were primarily involved in ion channel activity, protein transport, the oxytocin signalling pathway, neuroactive ligand-receptor interactions, and other signalling pathways. Based on the PPI network, ten hub genes (CHN2, OLIG2, UGT8A, CACNB2, TIMP3, FKBP5, ZBTB16, TSC22D3, ISL1, and SLC2A1) were checked. In the data set GSE7762, all of the Area Under Curve (AUC) values for the hub gene Receiver Operating Characteristic (ROC) curves were greater than 0.8. We also used the DGIdb database to look for eight small-molecule drugs that might be useful for treating morphine addiction. Conclusions: The hub genes are crucial genes associated with morphine addiction in the mouse striatum. The oxytocin signalling pathway may play a vital role in developing morphine addiction. [ABSTRACT FROM AUTHOR]

Objective: This study aimed to investigate the prevalence and correlates of food insufficiency and its association with mental disorders and adverse childhood experiences (ACE) in Singapore. Design: This analysis utilised data from the Singapore Mental Health Study (SMHS 2016). Setting: SMHS 2016 was a population-based, psychiatric epidemiological study conducted among Singapore residents. Participants: Interviews were conducted with 6126 respondents. Respondents were included if they were aged 18 years and above, Singapore citizens or permanent residents and able to speak in English, Chinese or Malay. Results: The prevalence of food insufficiency was 2·0 % (95 % CI (1·6, 2·5)) among adult Singapore residents. Relative to respondents who did not endorse any ACE, those with ACE (OR: 2·9, 95 % CI (1·2, 6·6)) had higher odds of food insufficiency. In addition, there were significant associations between lifetime mental disorders and food insufficiency. Bipolar disorder (OR: 2·7, 95 % CI (1·2, 6·0)), generalised anxiety disorder (OR: 4·5, 95 % CI (1·5, 13·5)) and suicidal behaviour (OR: 2·37, 95 % CI (1·04, 5·41)) were shown to be significantly associated with higher odds of food insufficiency. Conclusions: The prevalence of food insufficiency is low in Singapore. However, this study identifies a vulnerable group of food-insufficient adults that is significantly associated with mental disorders, including suicidality. Government-funded food assistance programmes and multi-agency efforts to deal with the social determinants of food insufficiency, such as income sufficiency and early detection and intervention of mental distress, are key to ensuring a sustainable and equitable food system. [ABSTRACT FROM AUTHOR]

The mechanism of Long Covid (Post-Acute Sequelae of COVID-19; PASC) is currently unknown, with no validated diagnostics or therapeutics. SARS-CoV-2 can cause disseminated infections that result in multi-system tissue damage, dysregulated inflammation, and cellular metabolic disruptions. The tissue damage and inflammation has been shown to impair microvascular circulation, resulting in hypoxia, which coupled with virally-induced metabolic reprogramming, increases cellular anaerobic respiration. Both acute and PASC patients show systemic dysregulation of multiple markers of the acid-base balance. Based on these data, we hypothesize that the shift to anaerobic respiration causes an acid-base disruption that can affect every organ system and underpins the symptoms of PASC. This hypothesis can be tested by longitudinally evaluating acid-base markers in PASC patients and controls over the course of a month. If our hypothesis is correct, this could have significant implications for our understanding of PASC and our ability to develop effective diagnostic and therapeutic approaches. [ABSTRACT FROM AUTHOR]

Objective: We evaluated associations between food insecurity (FI) and the quality and quantity of sleep in adults (≥18 years).Design: The current study represented a systematic review and meta-analysis of observational studies.Setting: Databases of PubMed, Scopus, Embase, and Web of Science were searched from inception until June 06, 2022. Meta-analyses were conducted using random-effects models, and effect sizes were reported as odds ratios (OR) and 95% confidence intervals (CI).Subjects: Data from ten eligible observational studies, including 83,764 participants, were included.Results: FI was associated with an increased risk of poor sleep quality (OR=1.45; 95% CI:1.24-1.70, I2 =95, P<0.001, n=7). Besides, subgroup analysis showed increased risk of poor sleep quality corresponding to the severity of FI across mild (OR=1.31; 95% CI: 1.16-1.48, I2 =0%, P<0.001, n=5), moderate (OR=1.49; 95% CI: 1.32-1.68, I2 =0%, P<0.001, n=5), and severe (OR=1.89; 95% CI: 1.63-2.20, I2 =0%, P<0.001, n=5) levels. Similarly, subgroup analysis by sleep problems showed that FI was associated with an increased the risk of trouble falling asleep (OR=1.39; 95% CI: 1.05-1.83, I2 =91%, P=0.002, n=3) and trouble staying asleep (OR=1.91; 95% CI: 1.37-2.67, I2 =89%, P<0.001, n=3). Moreover, FI was associated with the odds of shorter (OR=1.14; 95% CI:1.07-1.21, I2 =0%, P<0.001, n=4) and longer sleep duration (OR=1.14; 95% CI:1.03-1.26, I2 =0%, P=0.010, n=4).Conclusions: Collective evidence supports that FI is associated with poor sleep quality and quantity in adults. Preventative and management strategies that address FI may provide health benefits beyond improving nutritional status per se. [ABSTRACT FROM AUTHOR]

Background: Treatment-resistant depression (TRD) is a condition in a subset of depressed patients characterized by resistance to antidepressant medications. The global prevalence of TRD has been steadily increasing, yet significant advancements in its diagnosis and treatment remain elusive despite extensive research efforts. The precise underlying pathogenic mechanisms are still not fully understood. Epigenetic mechanisms play a vital role in a wide range of diseases. In recent years, investigators have increasingly focused on the regulatory roles of miRNAs in the onset and progression of TRD. miRNAs are a class of noncoding RNA molecules that regulate the translation and degradation of their target mRNAs via interaction, making the exploration of their functions in TRD essential for elucidating their pathogenic mechanisms., Methods and Results: A systematic search was conducted in four databases, namely PubMed, Web of Science, Cochrane Library, and Embase, focusing on studies related to treatment-resistant depression and miRNAs. The search was performed using terms individually or in combination, such as "treatment-resistant depression," "medication-resistant depression," and "miRNAs." The selected articles were reviewed and collated, covering the time period from the inception of each database to the end of February 2024. We found that miRNAs play a crucial role in the pathophysiology of TRD through three main aspects: 1) involvement in miRNA-mediated inflammatory responses (including miR-155, miR-345-5p, miR-146a, and miR-146a-5p); 2) influence on 5-HT transport processes (including miR-674,miR-708, and miR-133a); and 3) regulation of synaptic plasticity (including has-miR-335-5p,has-miR- 1292-3p, let-7b, and let-7c). Investigating the differential expression and interactions of these miRNAs could contribute to a deeper understanding of the molecular mechanisms underlying TRD., Conclusions: miRNAs might play a pivotal role in the pathogenesis of TRD. Gaining a deeper understanding of the roles and interrelations of miRNAs in TRD will contribute to elucidating disease pathogenesis and potentially provide avenues for the development of novel diagnostic and therapeutic strategies., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Depression is a common mental illness. However, its current treatments, like selective serotonin reuptake inhibitors (SSRIs) and micro-dosing ketamine, are extremely variable between patients and not well understood. Three neurotransmitters: serotonin, histamine, and glutamate, have been proposed to be key mediators of depression. This review focuses on analytical methods to quantify these neurotransmitters to better understand neurological mechanisms of depression and how they are altered during treatment. To quantitatively measure serotonin and histamine, electrochemical techniques such as chronoamperometry and fast-scan cyclic voltammetry (FSCV) have been improved to study how specific molecular targets, like transporters and receptors, change with antidepressants and inflammation. Specifically, these studies show that different SSRIs have unique effects on serotonin reuptake and release. Histamine is normally elevated during stress, and a new inflammation hypothesis of depression links histamine and cytokine release. Electrochemical measurements revealed that stress increases histamine, decreases serotonin, and leads to changes in cytokines, like interleukin-6. Biosensors can also measure non-electroactive neurotransmitters, including glutamate and cytokines. In particular, new genetic sensors have shown how glutamate changes with chronic stress, as well as with ketamine treatment. These techniques have been used to characterize how ketamine changes glutamate and serotonin, and to understand how it is different from SSRIs. This review briefly outlines how these electrochemical techniques work, but primarily highlights how they have been used to understand the mechanisms of depression. Future studies should explore multiplexing techniques and personalized medicine using biomarkers in order to investigate multi-analyte changes to antidepressants., (© 2024. The Author(s).)

Previous magnetic resonance studies of the dorsal hippocampus in male rats selected for aggressive attitude toward humans revealed lower contents of γ-aminobutyric acid (GABA), N-acetylaspartate, and creatinine+phosphocreatinine (Cr+PCr), as well as a higher of phosphorylethanolamine content, as compared to males selected for tame behavior. The effect of early social instability on the hippocampal volume and spectrum of neurometabolites in the dorsal hippocampus was investigated in adult tame, aggressive, and unselected gray rats Rattus norvegicus. Experimental conditions of social instability included early weaning, subsequent housing of behaviorally matched males in pairs until the age of 3 months, and daily replacement of cagemates from days 19 to 25. In the control group, rat pups were weaned at the age of 30 days and then kept by 4–5 animals per cage until the age of 3 months. Control aggressive males were inferior to tame counterparts in hippocampal volumes, both absolute and normalized to individual brain volumes, while early social instability had no effect on these indices. In experimental groups, lower phosphorylethanolamine and higher alanine contents in the dorsal hippocampus, as compared to control animals, were detected in aggressive males only. This fact may be due to a lower level of stress response in these animals, as we observed previously. From the obtained results, it follows that aggressive rats are more sensitive to social instability conditions. Moreover, the early instability conditions and selection for aggressive behavior oppositely affect both phosphorylethanolamine metabolism and integral characteristics of the metabolic profile in the dorsal hippocampus. [ABSTRACT FROM AUTHOR]

Adult hippocampal neurogenesis (AHN) is crucial for learning, memory, and emotion. Deficits of AHN may lead to reduced cognitive abilities and neurodegenerative disorders, such as Alzheimer's disease. Extensive studies on rodent AHN have clarified the developmental and maturation processes of adult neural stem/progenitor cells. However, to what extent these findings apply to primates remains controversial. Recent advances in next-generation sequencing technologies have enabled in-depth investigation of the transcriptome of AHN-related populations at single-cell resolution. Here, we summarize studies of AHN in primates. Results suggest that neurogenesis is largely shared across species, but substantial differences also exist. Marker gene expression patterns in primates differ from those of rodents. Compared with rodents, the primate hippocampus has a higher proportion of immature dentate granule cells and a longer maturation period of newly generated granule cells. Future research on species divergence may deepen our understanding of the mechanisms underlying adult neurogenesis in primates. [ABSTRACT FROM AUTHOR]

The current narrative review summarizes and examines several theories of panic disorder (PD) including biological theories, encompassing neurochemical factors, metabolic and genetic theories, respiratory and hyperventilation theories and cognitive theory. Biological theories have informed the development of psychopharmacological treatments; however, they may be limited in their utility given the efficacy of psychological treatments. In particular, behavioral and, more recently, cognitive models have garnered support due to the efficacy of cognitive-behavior therapy (CBT) in treating PD. The role of combination treatments has been found to be superior in the treatment of PD in particular cases, lending support for the need for an integrated approach and model for PD given that the etiology of PD is complex and multifactorial. [ABSTRACT FROM AUTHOR]

Multiple sclerosis (MS) is an autoimmune demyelinating disease of the central nervous system (CNS). Anxiety and depression are the most common psychiatric comorbidities of MS, which seriously affect patients' quality of life, treatment compliance, and prognosis. However, current treatments for anxiety and depression in MS show low therapeutic efficacy and significant side effects. In the present study, we explored the therapeutic effects of a novel low-toxic anti-inflammatory drug, nanoparticulate magnesium hydride (MgH2), on mood disorders of MS. We observed that anxiety/depression-like behaviors in experimental autoimmune encephalomyelitis (EAE) mice were alleviated by MgH2 treatment. In addition, disease severity and inflammatory demyelination were also diminished. Furthermore, we confirmed the suppressive effect of MgH2 on depression in the acute restraint stress model. Mechanistically, MgH2 may play a therapeutic role by promoting microglial M2 polarization, inhibiting microglial M1 polarization, and reducing oxidative stress and mitochondrial damage. Therefore, nanoparticulate MgH2 may be a promising therapeutic drug for psychiatric comorbidities of MS. [ABSTRACT FROM AUTHOR]

This study investigated the associations of relationship satisfaction, depression, and anxiety post-acute coronary syndrome in a sample of men having completed an early, couple-focused, and men-tailored psychoeducation intervention. A baseline sample of 50 male patients were followed over a 12-month period and completed the Couples Satisfaction Index and the Depression, Anxiety and Stress Scale. Results revealed a significant improvement in depression symptoms from T0 to T1, during which all participants completed the MindTheHeart® psychoeducation intervention. In addition, a hierarchical regression analysis showed that relationship satisfaction is an important predictor of this improvement in depression symptoms. Our preliminary findings point to the consideration of life partners in post-ACS interventions and encourage the exploration of this clinical approach in future research. [ABSTRACT FROM AUTHOR]

Macrophage migration inhibitory factor (MIF) is a pro‐inflammatory cytokine that represents a link between diet‐induced inflammation and insulin resistance. Our aim was to examine whether fructose diet affects inflammation and insulin signaling in the prefrontal cortex (PFC) of Mif knockout mice (MIF‐KO), and their possible link to neural plasticity and behavior. We analyzed nuclear factor κB (NF‐κB) and glucocorticoid signaling, expression of F4/80, IL‐1β, TNF‐α, TLR‐4, MyD88, arginase 1 (Arg‐1), mannose receptor (Mrc‐1), and leukemia inhibitory factor (Lif) to assess inflammation in the PFC of C57/BL6J and MIF‐KO mice consuming 20% fructose solution for 9 weeks. Insulin receptor (IR), IRS‐1 serine phosphorylations (307 and 1101) and activity of PKCα, Akt, GSK‐3β and AMPKα were used to analyze insulin signaling. Brain‐derived neurotrophic factor (BDNF) and insulin‐like growth factor 1 (IGF‐1) mRNA levels, together with synapthophysin and PSD‐95 protein level and calcium calmodulin‐dependent kinase 2 (CaMKII) activity, were used as plasticity markers. Behavior was examined in elevated plus maze, light dark box and novel object recognition test. The results showed concomitant increase of Tnf‐α, Tlr‐4, MyD88 and M2 microglia markers (Arg‐1, Mrc‐1, Lif) in the PFC of MIF‐KO, paralleled with unchanged glucocorticoid and insulin signaling. Increase of BDNF and IGF‐1 was paralleled with increased CaMKII activity, decreased PSD‐95 protein level, anxiogenic behavior, and impaired memory in MIF‐KO mice. Fructose feeding restored these parameters in the PFC to the control level and mitigated behavioral changes, suggesting that ameliorating effects of fructose on neuroinflammation and behavior depend on the presence of MIF. [ABSTRACT FROM AUTHOR]

Aim: Somatic symptom disorder (SSD) is a psychiatric disorder with unknown etiopathogenesis that is still under investigation. The results of neuroimaging studies on SSD have shown that some brain regions may be associated with it. In this connection, this study aims to explore the orbitofrontal cortex (OFC) morphometric changes in patients with SSD to better comprehend the etiopathogenesis. Material and Methods: The study enrolled 20 patients and 20 healthy controls. All study participants were administered a sociodemographic and clinical questionnaire, the Hamilton Depression Rating Scale (HAM-D) and the Hamilton Anxiety Rating Scale (HAM-A). The volumes of total brain, OFC, total white matter, and total gray matter were measured by a magnetic resonance imaging (MRI)-based method in studied patients. Results: Orbitofrontal cortex volume was significantly smaller in the patient group than in healthy controls (p<0.05). No significant difference between the two groups could be observed in total brain, white matter and gray matter volumes (p>0.05). Conclusions: The OFC was markedly smaller in SSD patients than in healthy controls, suggesting that the OFC may be associated with SSD pathophysiology. Future studies examining the functional features of the OFC using imaging and cognitive function tests will likely shed more light on this issue. [ABSTRACT FROM AUTHOR]

Background: Considering the huge population in China, the available mental health resources are inadequate. Thus, our study aimed to evaluate whether mental questionnaires, serving as auxiliary diagnostic tools, have efficient diagnostic ability in outpatient psychiatric services. Methods: We conducted a retrospective study of Chinese psychiatric outpatients. Altogether 1,182, 5,069, and 4,958 records of SymptomChecklist-90 (SCL-90), Hamilton Anxiety Rating Scale (HAM-A), and Hamilton Depression Rating Scale (HAM-D), respectively, were collected from March 2021 to July 2022. The Mann-Whitney U test was applied to subscale scores and total scores of SCL-90, HAM-A, and HAM-D between the two sexes (male and female groups), different age groups, and four diagnostic groups (anxiety disorder, depressive disorder, bipolar disorder, and schizophrenia). Kendall's tau coefficient analysis and machine learning were also conducted in the diagnostic groups. Results: We found significant differences in most subscale scores for both age and gender groups. Using the Mann-Whitney U test and Kendall's tau coefficient analysis, we found that there were no statistically significant differences in diseases in total scale scores and nearly all subscale scores. The results of machine learning (ML) showed that for HAM-A, anxiety had a small degree of differentiation with an AUC of 0.56, while other diseases had an AUC close to 0.50. As for HAM-D, bipolar disorder was slightly distinguishable with an AUC of 0.60, while the AUC of other diseases was lower than 0.50. In SCL-90, all diseases had a similar AUC; among them, bipolar disorder had the lowest score, schizophrenia had the highest score, while anxiety and depression both had an AUC of approximately 0.56. Conclusion: This study is the first to conduct wide and comprehensive analyses on the use of these three scales in Chinese outpatient clinics with both traditional statistical approaches and novel machine learning methods. Our results indicated that the univariate subscale scores did not have statistical significance among our four diagnostic groups, which highlights the limit of their practical use by doctors in identifying differentmental diseases in Chinese outpatient psychiatric services. [ABSTRACT FROM AUTHOR]

Background: Patients with panic disorder (PD) have an abnormal function in brain regions related to fear network is well recognised. However, the traditional fear network model (FNM) which was based on animals' horrible behaviours has been found that it's not enough to explain the pathological mechanism of PD. This study aims to explore brain regions' abnormalities in the new advanced FNM, and estimate whether it can better explain PD. Methods: Magnetic resonance imaging resting-state scans were acquired in 40 patients with PD (35 drug-naïve and 5 drug-free) and 40 healthy controls (HCs). Twelve brain regions in the advanced FNM were chosen as regions of interest (ROIs) to examine the group difference in the ROIs and whole-brain resting-state functional connectivity (rsFC). Results: We found significantly increased thalamic rsFC with the insula, compared with HCs. And it was significantly correlated with HAMA-somatic score. We also found increased thalamic rsFC with occipital gyrus, temporal gyrus, and frontal gyrus when compared with HCs. Conclusions: Taken together, PD patients exhibit abnormal rsFC alterations within the advanced FNM, especially the increased rsFC within thalamus-insula loop, suggesting that excessive sensitivity to external information plays an important role in PD. The advanced FNM may provide a fuller explanation about PD. [ABSTRACT FROM AUTHOR]

Purpose: During the juvenile stage, such areas as the hippocampus and corpus callosum (CC) are still immature and sensitive to stress exposure. The present study investigated whether two different types of stressors in the juvenile stage of life have a long-lasting impact on behavior and biological outcomes in adult rats. Methods: Male juvenile rats were exposed to restraint or predator stress on postnatal day 25 (P25) for 3 days. Thirty-two days later (P60-74), behavioral and biological analyses were conducted. The behavioral analysis included measures of anxiety-like behavior and recognition memory. The biological analysis investigated gross cerebral morphology, based on volume analysis of the CC and hippocampus, perirhinal cortex thickness, and dendritic spine density. Results: Neither restraint stress nor predator stress affected anxiety-like behavior or object recognition memory in adulthood. Body weight and adrenal gland weight were unaffected by both types of stress. Overall, volumetric measures of the CC and hippocampus were not significant, with no changes in perirhinal cortex thickness. Spine density in the medial prefrontal cortex also was unaffected, but a decrease in dendritic spine density was found in the hippocampus in response to restraint stress and an increase to predator stress. Conclusion: Short-term and daily restraint and predator stress during the juvenile stage had no long-lasting effects on anxiety-like behavior, object memory, volume of the CC or hippocampus, or perirhinal cortex thickness, but a decrease in dendritic spine density was found in the hippocampus. These findings suggest that different types of stressors have different impacts on microstructures in the brain without affecting behavior or the gross morphology of stress-sensitive brain areas. [ABSTRACT FROM AUTHOR]

The mother–child relationship of newborns plays an essential role in the development of the central nervous system, and an inadequate relationship, such as mother–child separation, can cause deficits of mental function in adulthood. However, insufficient research has examined the effects of foster mothers. We assigned some neonatal rats to one of two foster mothers: one that was lactating and feeding her first litter (FL group) and one that had one previous experience of childbirth and feeding but no current litter (FE group). Other pups were raised by their own mother (OM group) or subjected to maternal separation (MS group). Pups were placed with the foster mother (FL and FE groups) or separated from their mother (MS group) for 3 h/day on postnatal days 1–20. At age 6 weeks, each group was divided into two subgroups, one with 30 min of acute restraint stress loading (FL-R, FE-R, OM-R, and MS-R) and one without it (FL, FE, OM, and MS). Then, we compared the density of corticotropin-releasing factor-immunoreactive (CRF-ir) neurons in the central amygdaloid nucleus (CeA). The density of CRF-ir neurons in the CeA was significantly lower in the FL-R and MS-R subgroups than in the FL and MS subgroups, respectively. The results suggest that differences in care received during the neonatal period affect maturation of CRF neurons in the CeA and may have negative effects on the synthesis and release of CRF. [ABSTRACT FROM AUTHOR]

There is a growing interest in the psychiatric properties of the dissociative anaesthetic ketamine, as single doses have been shown to have fast‐acting mood‐enhancing and anxiolytic effects, which persist for up to a week after the main psychoactive symptoms have diminished. Therefore, ketamine poses potential beneficial effects in patients with refractory anxiety disorders, where other conventional anxiolytics have been ineffective. Ketamine is a noncompetitive antagonist of the N‐methyl‐d‐aspartate (NMDA) glutamate receptor, which underlies its induction of pain relief and anaesthesia. However, the role of NMDA receptors in anxiety reduction is still relatively unknown. To fill this paucity in the literature, this systematic review assesses the evidence that ketamine significantly reduces refractory anxiety and discusses to what extent this may be mediated by NMDA receptor antagonism and other receptors. We highlight the temporary nature of the anxiolytic effects and discuss the high discrepancy among the study designs regarding many fundamental factors such as administration routes, complementary treatments and other treatments. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the prevalence and predictors of perceived helpfulness of treatment in persons with a history of DSM-IV social anxiety disorder (SAD), using a worldwide population-based sample. Methods: The World Health Organization World Mental Health Surveys is a coordinated series of community epidemiological surveys of non-institutionalized adults; 27 surveys in 24 countries (16 in high-income; 11 in low/middle-income countries; N = 117,856) included people with a lifetime history of treated SAD. Results: In respondents with lifetime SAD, approximately one in five ever obtained treatment. Among these (n = 1322), cumulative probability of receiving treatment they regarded as helpful after seeing up to seven professionals was 92.2%. However, only 30.2% persisted this long, resulting in 65.1% ever receiving treatment perceived as helpful. Perceiving treatment as helpful was more common in female respondents, those currently married, more highly educated, and treated in non-formal health-care settings. Persistence in seeking treatment for SAD was higher among those with shorter delays in seeking treatment, in those receiving medication from a mental health specialist, and those with more than two lifetime anxiety disorders. Conclusions: The vast majority of individuals with SAD do not receive any treatment. Among those who do, the probability that people treated for SAD obtain treatment they consider helpful increases considerably if they persisted in help-seeking after earlier unhelpful treatments. [ABSTRACT FROM AUTHOR]

Ghrelin is known to be a feeding stimulatory hormone in mammals, but in birds, in contrast to mammals, the feeding behavior is regulated in inhibitory manners. This is because the neuropeptides associated with the regulation in the brain are different from those in mammals, i.e., it has been shown that, in chickens, a corticotropin-releasing hormone family peptide, urocortin, which is a feeding-inhibitory peptide, is mainly involved in the inhibitory mechanism. However, feeding is also regulated by various neurotransmitters in the brain, and recently, their interaction with the mechanisms underlying feeding inhibition by ghrelin in birds has been intensively studied and clarified. This review summarizes these findings.

Rationale: Using routine synthetic drugs in the treatment of psychiatric disorders may have some restrictions due to serious side effects and pharmacoresistance. Some natural agents may be promising alternatives in this case. The neuroprotective activity of the neuromodulator adenosine and its receptor, A 1 receptor (A 1 R) in the central nervous system has been mentioned in different studies., Objective: We aimed to determine the anxiolytic, antidepressant and sedative effects of Japanese sake yeast as the first report., Method: Mice were subjected to a one-week stress protocol and concomitantly treated orally with sake yeast at the dose levels of 100, 200 and 300 mg kg -1 once daily for a week. The anxiolytic, antidepressant, and sedative actions of sake yeast were evaluated with the related tests., Results: In all dose regiments, sake yeast significantly improved functions in the EPM and FST. 200 and 300 mg/kg of sake yeast significantly increased sleep duration and reduced sleep latency. Anxiolytic and antidepressant-like activities of sake yeast were maintained by the injection of ZM241385 (15 mg kg -1 ), a selective adenosine A 2A R antagonist but completely counteracted by the injection of 8-cyclopentyltheophylline (10 mg kg -1 ), a selective adenosine A 1 R antagonist. 300 mg/kg of the yeast significantly increased the BDNF levels. Amygdala corticosterone levels did not show any significant changes at any dosage. Amygdala TNF-α, IL-6 and IL-1β levels also decreased significantly with all the sake regiments compared to the control group., Conclusions: We conclude that oral sake yeast supplement exerts a neurobehavioral protective effect predominantly by activating central A 1 Rs., (© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

We have known for nearly a century that triggering seizures can treat serious mental illness, but what we do not know is why. Electroconvulsive Therapy (ECT) works faster and better than conventional pharmacological interventions; however, those benefits come with a burden of side effects, most notably memory loss. Disentangling the mechanisms by which ECT exerts rapid therapeutic benefit from the mechanisms driving adverse effects could enable the development of the next generation of seizure therapies that lack the downside of ECT. The latest research suggests that this goal may be attainable because modifications of ECT technique have already yielded improvements in cognitive outcomes without sacrificing efficacy. These modifications involve changes in how the electricity is administered (both where in the brain, and how much), which in turn impacts the characteristics of the resulting seizure. What we do not completely understand is whether it is the changes in the applied electricity, or in the resulting seizure, or both, that are responsible for improved safety. Answering this question may be key to developing the next generation of seizure therapies that lack these adverse side effects, and ushering in novel interventions that are better, faster, and safer than ECT., (© 2023. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.)

The article highlights a study on the effects of intra-ventral hippocampal memantine administration in male NMRI stressed mice were studied. It could be concluded that N-Methyl-D-aspartic acid glutamate receptors in the ventral hippocampus may play a pivotal role in the mediation of maintenance of anxiety and depression induced by stress in the mice.

Few studies have investigated the relationship between electroconvulsive therapy (ECT) and markers of nitrosative stress and oxidative DNA damage. The aim of this study is to examine changes in nitrosative stress and oxidative DNA damage in patients with a depressive episode treated with ECT. The current study included 48 patients with a depressive episode treated with ECT and 30 healthy control participants. First, the serum nitrosative stress markers of nitric oxide (NO•), nitric oxide synthase (NOS), and peroxynitrite (ONOO-) and the oxidative DNA damage marker 8-hydroxy-2′-deoxyguanosine (8-OHdG) were compared between the study and control groups. These parameters were also compared pre- and post-treatment for the study group. NO•, NOS, and ONOO- levels were significantly higher in patients with depressive disorder (DD) than in the control group. NO• and NOS levels significantly decreased in the ECT group after treatment while 8-OHdG levels significantly increased. The study findings suggest that ECT may have reduced nitrosative stress levels while increasing oxidative DNA damage. More research is now needed to better understand the issue. Nitrosative stress levels can increase in patients with depressive disorder. Electroconvulsive therapy may reduce nitrosative stress while increasıng oxidative DNA damage. These results suggest that nitrosative stress plays an important role in the mechanism of action of electroconvulsive therapy. [ABSTRACT FROM AUTHOR]

The breathing process possesses a complex variability caused in part by the respiratory central pattern generator in the brainstem; however, it also arises from chemical and mechanical feedback control loops, network reorganization and network sharing with nonrespiratory motor acts, as well as inputs from cortical and subcortical systems. The notion that respiratory fluctuations contain hidden information has prompted scientists to decipher respiratory signals to better understand the fundamental mechanisms of respiratory pattern generation, interactions with emotion, influences on the cortical neuronal networks associated with cognition, and changes in variability in healthy and disease-carrying individuals. Respiration can be used to express and control emotion. Furthermore, respiration appears to organize brain-wide network oscillations via cross-frequency coupling, optimizing cognitive performance. With the aid of information theory-based techniques and machine learning, the hidden information can be translated into a form usable in clinical practice for diagnosis, emotion recognition, and mental conditioning. [ABSTRACT FROM AUTHOR]

Social anxiety is a symptom widely prevalent among young adults, and when present in excess, can lead to maladaptive patterns of social behavior. Recent approaches that incorporate brain functional radiomic features and machine learning have shown potential for predicting certain phenotypes or disorders from functional magnetic resonance images. In this study, we aimed to predict the level of social anxiety in young adult participants by training machine learning models with resting-state brain functional radiomic features including the regional homogeneity, fractional amplitude of low-frequency fluctuation, fractional resting-state physiological fluctuation amplitude, and degree centrality. Among the machine learning models, the XGBoost model achieved the best performance with balanced accuracy of 77.7% and F1 score of 0.815. Analysis of input feature importance demonstrated that the orbitofrontal cortex and the degree centrality were most relevant to predicting the level of social anxiety among the input brain regions and the input type of radiomic features, respectively. These results suggest potential validity for predicting social anxiety with machine learning of the resting-state brain functional radiomic features and provide further understanding of the neural basis of the symptom. [ABSTRACT FROM AUTHOR]

Background: Over the last decades, brain surgery became a more frequently applied treatment for temporal lobe epilepsy (TLE). Despite its success, several studies found de-novo post-operative psychiatric symptoms in TLE surgery patients. Cognitive behavioural therapy is effective to treat brain healthy psychiatric patients but might not be translatable to patients with resections in emotion regulating networks as these areas seem to be essentially involved in successful psychotherapeutic treatment. Methods: Here we report the case of a female patient with medically refractory medial temporal lobe epilepsy resulting in left anterior temporal lobectomy at age 35. Post operation she did not show adequate fearful response but at the same time manifested symptoms of a severe panic disorder. We investigated if this patient, despite lesions in emotion-behaviour brain circuits, can benefit from cognitive behavioural therapy. Results: The intervention, customized to the specific resources and difficulties of the patient, was effective in stopping panic attacks and improving social functioning. Conclusions: This case shows that MTL brain surgery patients may benefit from CBT and demonstrates the important and if yet still somewhat mysterious role of the amygdala in emotion regulation processes. [ABSTRACT FROM AUTHOR]