Pathology Of Depression Research Articles

The Antidepressant Effect of Resveratrol Is Related to Neuroplasticity Mediated by the ELAVL4-Bdnf mRNA Pathway

Resveratrol, a plant-derived polyphenol, exhibits significant antidepressant effects and notably enhances neuroplasticity in neurological diseases. However, whether the antidepressant function of resveratrol is related to neuroplasticity remains uncertain, and the underlying mechanisms is poorly understood. This study aims to investigate the role and mechanism of resveratrol in neuroplasticity in depression. Here, we adopted the chronic unpredictable mild stress (CUMS) model and resveratrol intervention by oral gavage. Thereafter, behavioral tests confirmed resveratrol’s antidepressant effect, and Nissl staining, Golgi staining, and Western blotting (WB) were employed to assess the neuronal plasticity. Moreover, proteomic analysis and WB were used to screen and identify the key proteins. To investigate the downstream target of ELAV-like RNA-binding protein 4 (ELAVL4) (one of candidate genes), the RNA Interactome Database and the National Center for Biotechnology Information databases were utilized to predict the targets of ELAVL4. Finally, Quantitative PCR, WB, and Immunofluorescence were used to verify the prediction. Our results indicate that resveratrol alleviates CUMS-induced depressive-like behaviors accompanied by the restoration of impaired hippocampal neuroplasticity. Then, proteomic analysis shows that 351 differentially expressed proteins (DEPs) decrease after CUMS, while 24 DEPs increase remarkably with the resveratrol treatment. Among which, ELAVL4 is downregulated by CUMS, simultaneously increasing after resveratrol intervention, which acts as a protective protein in this process. Finally, brain-derived neurotrophic factor (Bdnf) mRNA is predicted to be the potential target of ELAVL4 and validated by molecular technologies. In conclusion, our findings demonstrate that resveratrol’s antidepressant efficacy is closely associated with ELAVL4, an RNA-binding protein, a mediated neuroplasticity pathway, potentially intersecting with the Bdnf mRNA. Overall, this research sheds light on the role of the ELAVL4-Bdnf mRNA pathway through neuroplasticity in resveratrol’s antidepressant action, which provides an mRNA regulation perspective for the development of novel antidepressants and understanding depression pathology.

Myelin Repair as a Novel Mechanism for Ketamine's Sustained Antidepressant Effects.

Depression is a prevalent mental disorder, affecting approximately 300 million people worldwide. Despite decades of research into the underlying mechanisms of depression, a consensus remains elusive. Recent studies have implicated changes in oligodendrocytes and myelin in the pathogenesis of depression. Conventional antidepressants may alleviate symptoms within weeks of use, but approximately one-third of patients do not respond to them. Ketamine exhibits rapid and sustained antidepressant effects in treatment-resistant patients with depression. Given the association between reduced myelination and depression pathology, alterations in myelination may be a key mechanism underlying ketamine's prolonged antidepressant effects. However, the exact role of myelination in ketamine's sustained antidepressant effects remains unclear. In this review, we summarize the relationship between demyelination and depression and discuss the potential mechanisms by which ketamine may exert its antidepressant effects by repairing myelin damage, offering new insights into the role of myelination in antidepressant mechanisms.

Transcription factor Yy1 modulates Trem1 to control LPS-triggered neuroinflammation and oxidative stress in mouse astrocytes via the NF-κB pathway.

Dysfunction of astrocytes has a crucial role in the pathology of depression. Here, we aimed to define the exact action of the ubiquitous transcription factor (TF) Yin Yang-1 (Yy1) in depression pathogenesis and astrocytic dysfunction. A chronic unpredictable mild stress (CUMS) mouse model was generated. Primary mouse astrocytes were exposed to lipopolysaccharide (LPS). Cell growth was determined by CCK-8 and EdU assays. The direct interaction of Yy1 and the Trem1 promoter was validated by chromatin immunoprecipitation (ChIP) and luciferase assays. In CUMS mice, the levels of Yy1 and inflammatory cytokines were augmented and oxidative stress was enhanced. Functionally, disruption of Yy1 or triggering receptor expressed on myeloid cell 1 (Trem1) relieved LPS-triggered pro-growth, pro-inflammation, and pro-oxidative stress effects in mouse astrocytes. Mechanistically, Yy1 directly promoted the transcription and expression of Trem1 by binding to the Trem1 promoter. Yy1 disruption exerted regulatory impacts in LPS-induced mouse astrocytes via down-regulation of Trem1. Additionally, the Yy1/Trem1 cascade could modulate the activation of the NF-κB signaling in mouse astrocytes. Our study defines that Yy1 disruption relieves LPS-triggered neuroinflammation and oxidative stress in mouse astrocytes via the NF-κB pathway by down-regulating Trem1, providing possible strategies for depression treatment.

Inflammatory pathology in depression and suicide: a mechanistic distillation of clinical correlates

The association between inflammation with depression and suicide has prompted many investigations of the potential contributors to inflammatory pathology in these psychiatric illnesses. However, a distillation of diverse clinical findings into an integrated framework of the possible involvement of major physiological processes in the elicitation of pathological inflammation in depression and suicide has not yet been explored. Therefore, this review aims to provide a concise synthesis of notable clinical correlates of inflammatory pathology in subjects with various depressive and suicidal clinical subtypes into a mechanistic framework, which includes aberrant immune activation, deregulated neuroendocrine signaling, and impaired host-microbe interaction. These issues are of significant research interest as their possible interplays might be involved in the development of distinct subtypes of depression and suicide. We conclude the review with discussion of a pathway-focused therapeutic approach to address inflammatory pathology in these psychiatric illnesses within the realm of personalized care for affected patients.

Association of TyG Index and TG/HDL-C Ratio with Trajectories of Depressive Symptoms: Evidence from China Health and Retirement Longitudinal Study.

To explore whether the triglyceride-glucose (TyG) index and the triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio are associated with the trajectories of depressive symptoms. In this longitudinal study, 4215 participants aged 45 years and older were recruited from the China Health and Retirement Longitudinal Study from 2011 to 2018. The trajectories of depressive symptoms, measured by the 10-item Center for Epidemiologic Studies Depression Scale (CESD-10), were identified using group-based trajectory modeling. Multinomial logistic models and restricted cubic spline analysis were used to investigate the relationships between the TyG index and the TG/HDL-C ratio and the trajectories of depressive symptoms. Stratified analyses were conducted based on sex, age, place of residence, and body mass index (BMI). Five distinct trajectories of depressive symptoms characterized by stable low, stable moderate, decreasing, increasing, and stable high were identified during a follow-up of 7 years. The associations of the TyG index and the TG/HDL-C ratio with trajectories of depressive symptoms are not entirely consistent. After adjusting for covariates, a higher TyG index at baseline was associated with lower odds of being on the decreasing trajectory of depressive symptoms (ORad = 0.61, 95% CI: 0.40-0.92) compared to the stable low trajectory, and restricted cubic spline analysis revealed a negative linear relationship between the TyG index and the likelihood of a decreasing trajectory of depressive symptoms. However, the relationship between the TG/HDL-C ratio and the decreasing trajectory of depressive symptoms was no longer statistically significant when all confounders were controlled (ORad = 0.72, 95% CI: 0.50-1.04). Additionally, this negative association between the TyG index and decreasing trajectory of depressive symptoms was observed among 45-64-year-old individuals, female participants, those living in rural areas, and those with a normal BMI. This study was conducted in a middle-aged and elderly population in China, and extrapolation to other regions and populations requires further confirmation. Compared to the TG/HDL-C ratio, the TyG index may be a better predictor for trajectories of depressive symptoms in middle-aged and older adults. Considering that the pathology of depression progresses long term, our findings may have utility for identifying available and reliable markers for the development of depression.

Changes in hippocampal volume, 5-HT4 receptor binding, and verbal memory over the course of antidepressant treatment in major depressive disorder

Serotonin reuptake inhibitors have been reported to increase hippocampal volume and improve memory function in patients with Major depressive disorder (MDD). The postsynaptic 5-HT4 receptor (5-HT4R) is involved in hippocampal development, familial risk for depression and depressive pathology. In an open-label trial with 91 patients (72% female, mean 27.2 years) with MDD, we investigated the relation between changes in hippocampal volume, 5-HT4R, and verbal memory during 12 weeks treatment with 10–20 mg escitalopram. Depression severity, verbal memory, MRI-determined hippocampus volume and PET-determined 5-HT4R were measured pretreatment. Forty-three patients were rescanned at week 8. HAMD17 was reassessed at week 8 and together with verbal memory at week 12. We used mixed-effects models and linear regressions. We estimated a 27 mm3 (p = 0.086) reduction in mean hippocampus volume over the course of eight weeks. In patients clinically responding to treatment, we estimated a 45 mm3 reduction (p = 0.019), 8 mm3 increase in non-responders (p = 0.78), and a 52 mm3 group difference (p = 0.12). Hippocampal 5-HT4 receptor binding before treatment and at week eight was negatively associated with hippocampal volume in females, regardless of treatment response (p-values≤0.006). However, no clear evidence for an association in males or sex interaction could be established (p-values≥0.16). Although the hippocampus volume did not increase with treatment, we found a decrease in clinically responsive patients. Our findings suggest an association between 5-HT4R signalling and changes in hippocampal volume in females with MDD during antidepressant treatment, highlighting the need for further investigation into the role of serotonergic mechanisms in hippocampal plasticity.

MicroRNA-specific targets for neuronal plasticity, neurotransmitters, neurotrophic factors, and gut microbes in the pathogenesis and therapeutics of depression

Depression is of great concern because of the huge burden, and it is impacted by various epigenetic modifications, e.g., histone modification, covalent modifications in DNA, and silencing mechanisms of non-coding protein genes, e.g., microRNAs (miRNAs). MiRNAs are a class of endogenous non-coding RNAs. Alternations in specific miRNAs have been observed both in depressive patients and experimental animals. Also, miRNAs are highly expressed in the central nervous system and can be delivered to different tissues via tissue-specific exosomes. However, the mechanism of miRNAs' involvement in the pathological process of depression is not well understood. Therefore, we summarized and discussed the role of miRNAs in depression. Conclusively, miRNAs are involved in the pathology of depression by causing structural and functional changes in synapses, mediating neuronal regeneration, differentiation, and apoptosis, regulating the gut microbes and the expression of various neurotransmitters and BDNF, and mediating inflammatory and immune responses. Moreover, miRNAs can predict the efficacy of antidepressant medications and explain the mechanism of action of antidepressant drugs and aerobic exercise to prevent and assist in treating depression.

Luteolin ameliorates chronic stress-induced depressive-like behaviors in mice by promoting the Arginase-1+ microglial phenotype via a PPARγ-dependent mechanism.

Accumulating evidence shows that neuroinflammation substantially contributes to the pathology of depression, a severe psychiatric disease with an increasing prevalence worldwide. Although modulating microglial phenotypes is recognized as a promising therapeutic strategy, effective treatments are still lacking. Previous studies have shown that luteolin (LUT) has anti-inflammatory effects and confers benefits on chronic stress-induced depression. In this study, we investigated the molecular mechanisms by which LUT regulates the functional phenotypes of microglia in mice with depressive-like behaviors. Mice were exposed to chronic restraint stress (CRS) for 7 weeks, and were administered LUT (10, 30, 40 mg· kg-1 ·day-1, i.g.) in the last 4 weeks. We showed that LUT administration significantly ameliorated depressive-like behaviors and decreased hippocampal inflammation. LUT administration induced pro-inflammatory microglia to undergo anti-inflammatory arginase (Arg)-1+ phenotypic polarization, which was associated with its antidepressant effects. Furthermore, we showed that LUT concentration-dependently increased the expression of PPARγ in LPS + ATP-treated microglia and the hippocampus of CRS-exposed mice, promoting the subsequent inhibition of the NLRP3 inflammasome. Molecular dynamics (MD) simulation and microscale thermophoresis (MST) analysis confirmed a direct interaction between LUT and peroxisome proliferator-activated receptor gamma (PPARγ). By using the PPARγ antagonist GW9662, we demonstrated that LUT-driven protection, both in vivo and in vitro, resulted from targeting PPARγ. First, LUT-induced Arg-1+ microglia were no longer detected when PPARγ was blocked. Next, LUT-mediated inhibition of the NLRP3 inflammasome and downregulation of pro-inflammatory cytokine production were reversed by the inhibition of PPARγ. Finally, the protective effects of LUT, which attenuated the microglial engulfment of synapses and prevented apparent synapse loss in the hippocampus of CRS-exposed mice, were eliminated by blocking PPARγ. In conclusion, this study showed that LUT ameliorates CRS-induced depressive-like behaviors by promoting the Arg-1+ microglial phenotype through a PPARγ-dependent mechanism, thereby alleviating microglial pro-inflammatory responses and reversing microglial phagocytosis-mediated synapse loss.

Efficacy of Yoga in Reducing Depressive Symptoms: A Systematic Review

Introduction: The fast pace of changes in contemporary life increases the need to adapt, which leads to depressive pathologies due to psychological suffering. Yoga has therefore emerged as a complementary approach to the treatment of depression. Objective: To analyze the efficacy of yoga in reducing depressive symptoms. Materials and methods: This is a systematic literature review, which followed the Joanna Briggs Institute methodology for systematic reviews of efficacy, with the review protocol registered on Prospero under the code CRD42023448158. To devise the research question, the Pico strategy was adopted, in which “P” stands for people with depression, “I” for yoga; “C” for people who have not been submitted to yoga, and “O” for improvement/reduction of depressive symptoms. The requirements of the Prisma flowchart were followed and the search was conducted in the Medline/PubMed, Web of Science, Lilacs, BDEnf, Ibecs, PsycINFO, and Cinahl databases. The Jadad scale was used to assess methodological quality and the Cochrane Risk of Bias 2 to assess the risk of bias. Results: A total of 1138 studies were found, of which 10 were selected for data extraction, detailed reading, and qualitative synthesis. Yoga, especially mindfulness yoga, has been shown to be an effective intervention for various conditions, including depression. Its benefits include significant improvements in depression severity, health-related quality of life, motor dysfunction, mobility, spiritual well-being, and parasympathetic nervous system activity. Conclusion: The studies highlight the efficacy of yoga in reducing depressive symptoms in various populations and contexts, highlighting its effectiveness as a complementary therapeutic approach in the management of depression.

Brain Specific RagA Overexpression Triggers Depressive-Like Behaviors in Mice via Activating ADORA2A Signaling Pathway.

Neuroinflammation hallmarks the pathology of depression although the etiological complexity has not yet been resolved. Previous studies demonstrate that bacterial lipopolysaccharide induces depressive-like behaviors by activating RagA-mTOR-p70S6K signaling pathway. The current project aims to investigate whether and how brain-specific RagA overexpression triggers depressive-like behaviors in mice. Full-length RagA cDNA is cloned into the mammalian expression vector under the control of brain specific promoter, and subsequently overexpressed in the brain of mouse embryos. Indeed, RagA transgenic mice exhibit depressive-like behaviors and memory impairments. RNA-seq profiling of the prefrontal cortex (PFC) transcriptome highlights adenosine A2a receptor (ADORA2A) as a key differentially expressed gene (DEG). Western blotting confirms that ADORA2A and phospho-p70S6K are markedly elevated in RagA transgenic mice. Behavioral assessments demonstrate that ADORA2A inhibitor istradefylline markedly attenuates depressive-like behaviors. Further metabolomics reveals that N-acetylserotonin and several depression-related metabolites are downregulated while proteomic profiling showed that OLIG1 and other proteins are significantly regulated in RagA transgenic mice. Collectively, RagA overexpression alters the expression patterns of signaling proteins and the metabolism of depression-associated metabolites. RagA may cause depressive-like behaviors in mice via activating p70S6K/ADORA2A signaling pathway. Thus, RagA-p70S6K-ADORA2A signaling pathway may be a target for the development of new antidepressant therapies.

ANALYSE DES RISQUES SOCIO-ENVIRONNEMENTAUX DANS L’INDUSTRIE AGROALIMENTAIRE : APPLICATION DE LA METHODE AMDEC PROCESSUS AU SEIN DE BRACONGO SA (R.D. CONGO)

The manufacturing and production processes of beverages in the agro-industrial sector present a number of risks that can negatively impact the health and safety of employees as well as the environment. The aim of this study is to map the various socio-environmental risks of BRACONGO SA in order to establish an integrated HSE (Hygiene, Safety and Environment) management system to control these hazards in a continuous improvement context. To this end, the Failure Mode, Effects and Criticality Analysis (FMECA) method by process was used to identify and assess risks and classify them in a two-dimensional matrix (severity ans likelihood). The results obtained after calculating the criticality of risks show that environmental pollution (air and soil) has criticality coefficients of 16, while fire risks indicate a criticality of 6. Noise and ergonomic risks (stress, handling, musculoskeletal disorders, depressive pathologies) fall within the red zone of the risk matrix, which calls for the implementation of urgent actions. Current preventive or protective measures, such as personal or collective protective equipment, training, and infrastructures like wastewater treatment plants, are partially effective but insufficient for addressing certain major risks.

Investigating the genetic relationship of intracranial and subcortical brain volumes with depression and other psychiatric disorders

Abstract Depression is one of the most common mental health disorders worldwide, yet its neurobiological mechanisms remain poorly understood. Structural brain differences in subcortical limbic regions are thought to be implicated in the pathology of depression. We leveraged genome-wide association studies (GWAS) summary-level data to explore the molecular pathways underlying the relationship between genetic risk for depression and intracranial and subcortical brain volumes measured via magnetic resonance imaging. At the whole-genome level, we identified a negative genetic correlation (rG) between depression and the volume of the ventral diencephalon (rG = -0.08), which remained significant after adjusting for multiple testing. We observed nominal (P < 0.05) positive genetic correlations between depression and the volumes of the caudate nucleus (rG = 0.06) and the putamen (rG = 0.06), while hippocampal volume displayed a negative genetic correlation (rG = -0.06) with depression. Pairwise GWAS analyses uncovered 104 genome segments with genetic variants influencing the aetiology of depression and at least one brain volume at the local genetic level. Gene association analyses of these genomic segments suggest putative links with dopamine neurotransmission, mesocorticolimbic functional connectivity, GABAergic transmission, and the insulin signalling pathway. Sensitivity analyses showed that the volume of the ventral diencephalon is also negatively correlated with bipolar disorder and schizophrenia; however, most of the genes associated with depression and brain volumes are specific for depression and do not replicate when investigating bipolar disorder or schizophrenia with brain volumes. We observed negative phenotypic correlations between depression and intracranial and subcortical brain volumes. Overall, our findings contribute to our understanding of the neurobiology of depression and suggest that, besides the known role of the hippocampus, other subcortical structures might also play essential roles in the aetiology of depression.

Empagliflozin-activated AMPK elicits neuroprotective properties in reserpine-induced depression via regulating dynamics of hippocampal autophagy/inflammation and PKCζ-mediated neurogenesis

RationaleMajor depression has been an area of extensive research during the last decades, for it represents a leading cause of disability and suicide. The stark rise of depression rates influenced by life stressors, economic threats, pandemic era, and resistance to classical treatments, has made the disorder rather challenging. Adult hippocampal neurogenesis and plasticity are particularly sensitive to the dynamic interplay between autophagy and inflammation. In fact, the intricate balance between the two processes contributes to neuronal homeostasis and survival.ObjectivesHaving demonstrated promising potentials in AMPK activation, a major metabolic sensor and autophagy regulator, empagliflozin (Empa) was investigated for possible antidepressant properties in the reserpine rat model of depression.ResultsWhile the reserpine protocol elicited behavioral, biochemical, and histopathological changes relevant to depression, Empa outstandingly hindered these pathological perturbations. Importantly, hippocampal autophagic response markedly declined with reserpine which disrupted the AMPK/mTOR/Beclin1/LC3B machinery and, conversely, neuro-inflammation prevailed under the influence of the NLRP3 inflammasome together with oxidative/nitrative stress. Consequently, AMPK-mediated neurotrophins secretion obviously deteriorated through PKCζ/NF-κB/BDNF/CREB signal restriction. Empa restored hippocampal monoamines and autophagy/inflammation balance, driven by AMPK activation. By promoting the atypical PKCζ phosphorylation (Thr403) which subsequently phosphorylates NF-κB at Ser311, AMPK successfully reinforced BDNF/CREB signal and hippocampal neuroplasticity. The latter finding was supported by hippocampal CA3 toluidine blue staining to reveal intact neurons.ConclusionThe current study highlights an interesting role for Empa as a regulator of autophagic and inflammatory responses in the pathology of depression. The study also pinpoints an unusual contribution for NF-κB in neurotrophins secretion via AMPK/PKCζ/NF-κB/BDNF/CREB signal transduction. Accordingly, Empa can have special benefits in diabetic patients with depressive symptoms.LimitationsThe influence of p-NF-κB (Ser311) on NLRP3 inflammasome assembly and activation has not been investigated, which can represent an interesting point for further research.Graphical abstract

Behavioral Animal Models and Neural-Circuit Framework of Depressive Disorder.

Depressive disorder is a chronic, recurring, and potentially life-endangering neuropsychiatric disease. According to a report by the World Health Organization, the global population suffering from depression is experiencing a significant annual increase. Despite its prevalence and considerable impact on people, little is known about its pathogenesis. One major reason is the scarcity of reliable animal models due to the absence of consensus on the pathology and etiology of depression. Furthermore, the neural circuit mechanism of depression induced by various factors is particularly complex. Considering the variability in depressive behavior patterns and neurobiological mechanisms among different animal models of depression, a comparison between the neural circuits of depression induced by various factors is essential for its treatment. In this review, we mainly summarize the most widely used behavioral animal models and neural circuits under different triggers of depression, aiming to provide a theoretical basis for depression prevention.

The forensic aspects of suicide and neurotrophin factors: a research study.

Introduction: Suicide represents a significant public health problem whose neurobiology is not yet fully understood. In many cases, suicidal behavior and psychiatric spectrum disorders are linked, in particular, to major depression. An emerging pathophysiological hypothesis underlines the role of neurotrophic factors, proteins involved in neurogenesis, in synaptic plasticity in response to stressors. Our research aims to evaluate the degree of expression of brain neurotrophic factor (BDNF) in brain areas involved in depressive disorder in suicidal subjects. Furthermore, we want to evaluate the expression of glial cell line-derived neurotrophic factor (GDNF) in suicidal subjects. Methods: We selected twenty confirmed cases of suicide among subjects with a clinical history of depressive pathology and possible psychopharmacological treatment, compared to ten controls of individuals who died of non-suicidal causes. For all selected cases and controls, immunohistochemical investigations were performed using a panel of antibodies against the BDNF and GDNF antigens on samples from the various brain areas. Results and discussion: The results show that BDNF was under-expressed in the cerebral parenchyma of subjects who died by suicide compared to controls, while there was an overexpression of GDNF in suicide victims, these data could be useful for a clinical application as potential markers for suicidal risk, to assess the severity of depression and development of specific pharmacological therapies for depression.

Deciphering prefrontal circuits underlying stress and depression: exploring the potential of volume electron microscopy.

Adapting to environmental changes and formulating behavioral strategies are central to the nervous system, with the prefrontal cortex being crucial. Chronic stress impacts this region, leading to disorders including major depression. This review discusses the roles for prefrontal cortex and the effects of stress, highlighting similarities and differences between human/primates and rodent brains. Notably, the rodent medial prefrontal cortex is analogous to the human subgenual anterior cingulate cortex in terms of emotional regulation, sharing similarities in cytoarchitecture and circuitry, while also performing cognitive functions similar to the human dorsolateral prefrontal cortex. It has been shown that chronic stress induces atrophic changes in the rodent mPFC, which mirrors the atrophy observed in the subgenual anterior cingulate cortex and dorsolateral prefrontal cortex of depression patients. However, the precise alterations in neural circuitry due to chronic stress are yet to be fully unraveled. The use of advanced imaging techniques, particularly volume electron microscopy, is emphasized as critical for the detailed examination of synaptic changes, providing a deeper understanding of stress and depression at the molecular, cellular and circuit levels. This approach offers invaluable insights into the alterations in neuronal circuits within the medial prefrontal cortex caused by chronic stress, significantly enriching our understanding of stress and depression pathologies.

Understanding the Pathology of Major Depression in a Non-clinical Student Sample: The Role of Mental Pain, Cognitive Emotion Regulation, Self-Compassion, and Anxiety

Background: Severe psychological or mental pain is an experience of discomfort that can be associated with mental illness (such as major depression) or loss (such as the death of a child). Objectives: The aim of this study is to understand the pathology of major depression using a non-clinical student sample by assessing the roles of mental pain, cognitive emotion regulation, self-compassion, and anxiety. Methods: This cross-sectional study selected a sample (n = 300) using a multi-stage random cluster sampling method. Data was collected using the Orbach & Mikulincer Mental Pain Questionnaire (OMMP), the Cognitive Emotion Regulation Questionnaire (CERQ), the Self-Compassion Scale-Short Form (SCS-SF), the Beck Anxiety Inventory (BAI), and the Beck Depression Inventory-II (BD-II). Results: The results of the forward multiple linear regression model showed significant standardized beta coefficients for the following variables: Anxiety and depression (β = 0.21, P = 0.002), mental pain and depression (β = 0.436, P < 0.001), maladaptive cognitive emotion regulation strategies and depression (β = 0.21, P = 0.002), negative dimensions of self-compassion and depression (β = 0.082, p = 0.041), adaptive cognitive emotion regulation strategies and depression (β = -0.135, P = 0.031), and positive dimensions of self-compassion and depression (β = -0.078, P = 0.042). Additionally, the results indicated that 56% of the variance in depression is explained by mental pain, cognitive emotion regulation, self-compassion, and anxiety (P < 0.001). Conclusions: The results of this study indicate that therapies focused on emotional regulation and self-compassion can effectively address emotional problems, anxiety, and depression in individuals with depression.

Association of anxiety and depression with breast implant illness syndrome (BII): a prospective observational cross-sectional study

Introduction: Breast Implant Illness syndrome (BII), popularly known as “silicone disease”, has no defined pathophysiology or recognition by the WHO. It consists of systemic symptoms such as joint pain, muscle pain, confusion, memory loss/cognitive problems, chronic fatigue, and immune diseases. In some more recent studies, anxiety and depression have been observed as an incident characteristic of the syndrome. Objective: It was to relate the appearance of anxiety and depression pathologies with the development of Breast Implant Illness syndrome in women with breast implants. Methods: To prepare the following prospective observational cross-sectional study, 132 women who had breast implants were interviewed and answered an online questionnaire with 18 questions about the breast implant that was disseminated through social networks. To obtain the data, questions about pre-operative and post-operative signs and symptoms were crossed, this data was subsequently struck and finally, another cross was carried out with the other unknown, symptoms were diagnosed by doctors. Results: The validation analysis of the questionnaire proposed in this study using Cronbach's alpha (α) statistical technique showed that the reliability rating was high, with alpha (α)=0.82. It was noted that 31% of women who did not have any characteristic signs and symptoms presented after placement and of these 22 women were diagnosed by doctors. And at the other intersection, it was clear that 25% presented depression after the placement of the breast implant and 23 of these women were diagnosed by doctors. Conclusion: It can be stated that anxiety and depression are pathologies associated with Breast Implant Illness syndrome.

BIDIRECTIONAL INTERACTION OF BLOOD GLUCOSE AND MENTAL STATUS AND ITS ROLE IN DEVELOPING DIABETES MELLITUS AND PSYCHIATRIC DISORDERS – SYSTEMATIC REVIEW

Blood glucose concentration in certain situations affects current mental status. Anxiety occurring during hunger or lack of concentration associated with hypoglycemia are well-known phenomenon. Variations of glucose levels may also present a long-term impact on mental status and mental health. Moreover, impaired mental status leads to neglecting health-promoting life choices in some individuals, while psychiatric disorders may contribute much more to the development of metabolic diseases. Aims: The aim of this review is to assess the current state of knowledge about the bidirectional interaction of blood glucose levels, including its fluctuations and management, and mental status. Methods: In our publication we used scientific sources such as publications and textbooks. Results: Studies show the most significant correlation between diabetes and psychiatric disorders, mostly depression, but also indicate that healthy individuals may present a correlation of metabolic and mental disorders. Diabetic patients are more prone to develop psychiatric disorders, but also psychiatric patients are more commonly affected by diabetes mellitus. Moreover, those suffering from both diseases show the highest risk of overall mortality. Inflammatory pathology of both diabetes and depression, which is the most common psychiatric disorder in diabetic patients, suggests that chronic inflammation may play the main role in this relationship. Conclusion: Analyzing different risk factors of comorbidity, the significance of reversible ones is indisputable. Taking that into account, some lifestyle changes may be beneficial for metabolic and mental disorders prevention. Further studies could indicate certain pathological relationships and help understand the correlation between blood glucose and mental state in healthy individuals.

High-Order line graphs of fMRI data in major depressive disorder.

Resting-state functional magnetic resonance imaging (rs-fMRI) technology and the complex network theory can be used to elucidate the underlying mechanisms of brain diseases. The successful application of functional brain hypernetworks provides new perspectives for the diagnosis and evaluation of clinical brain diseases; however, many studies have not assessed the attribute information of hyperedges and could not retain the high-order topology of hypergraphs. In addition, the study of multi-scale and multi-layered organizational properties of the human brain can provide richer and more accurate data features for classification models of depression. This work aims to establish a more accurate classification framework for the diagnosis of major depressive disorder (MDD) using the high-order line graph algorithm. And accuracy, sensitivity, specificity, precision, F1 score are used to validate its classification performance. Based on rs-fMRI data from 38 MDD subjects and 28 controls, we constructed a human brain hypernetwork and introduced a line graph model, followed by the construction of a high-order line graph model. The topological properties under each order line graph were calculated to measure the classification performance of the model. Finally, intergroup features that showed significant differences under each order line graph model were fused, and a support vector machine classifier was constructed using multi-kernel learning. The Kolmogorov-Smirnov nonparametric permutation test was used as the feature selection method and the classification performance was measured with the leave-one-out cross-validation method. The high-order line graph achieved a better classification performance compared with other traditional hypernetworks (accuracy=92.42%, sensitivity=92.86%, specificity=92.11%, precision=89.66%, F1=91.23%). Furthermore, the brain regions found in the present study have been previously shown to be associated with the pathology of depression. This work validated the classification model based on the high-order line graph, which can better express the topological features of the hypernetwork by comprehensively considering the hyperedge information under different connection strengths, thereby significantly improving the classification accuracy of MDD. Therefore, this method has potential for use in the clinical diagnosis of MDD.