A growing body of research suggested that there was a link between poor periodontal health and systemic diseases, particularly with the early development of cognitive disorders, dementia, and depression. This is especially true in cases of changes in diet, malnutrition, loss of muscular endurance, and abnormal systemic inflammatory response. Our study aimed to determine the extent of these associations to better target the multi-level healthy aging challenge investigating the impact of periodontal disease on cognitive disorders (cognitive impairment and cognitive decline), dementia, and depression. We conducted a comprehensive literature search up to November 2023 using six different electronic databases. Two independent researchers assessed the eligibility of 7363 records against the inclusion criteria and found only 46 records that met the requirements. The study is registered on PROSPERO (CRD42023485688). We generated random effects pooled estimates and 95% confidence intervals (CI) to evaluate whether periodontal disease increased the risk of the investigated outcomes. The quality assessment revealed moderate quality of evidence and risk of bias. Periodontal disease was found to be associated with both cognitive disorders (relative risk (RR) 1.25, 95% CI 1.11-1.40, in the analysis of cross-sectional studies); cognitive impairment (RR 3.01, 95% CI 1.52-5.95 for longitudinal studies, cognitive decline); and dementia (RR 1.22, 95% CI 1.10-1.36). However, no significant increased risk of depression among subjects with periodontal disease was found (RR 1.07, 95% CI 0.95-1.21). Despite the association with two of the three explored outcomes, the available evidence on periodontal diseases and dementia, cognitive disorders, and depression is controversial due to several limitations. Therefore, further investigations involving validated and standardized tools are required.

Idiopathic Sudden Sensorineural Hearing Loss (ISSHL) is a sudden onset, unexplained sensorineural hearing loss. Depression is a common mental disorder and a leading cause of disability. Here, We used a two-sample Mendelian randomization approach using pooled statistics from genome-wide association studies of ISSHL (1491 cases, 196,592 controls) and depression (23,424 cases, 192,220 controls) in European populations. This study investigated the bidirectional relationship between single nucleotide polymorphisms associated with depression and ISSHL using inverse variance weighting.Additional sensitivity analyses, such as Mendelian randomization-Egger (MR-Egger), weighted median estimates, and leave-one-out analysis, were performed to assess the reliability of the findings. Significant causal association between genetic susceptibility to ISSHL and depression in a random-effects IVW approach (OR = 1.037, 95% CI = 1.004-1.072, P = 0.030). In contrast, genetic depression was not risk factors for ISSHL (OR = 1.134, 95% CI = 0.871-1.475, P = 0.350). After validation by different MR methods and the sensitivity analysis, all of the above results are consistent. The evidence we have gathered suggests a causal relationship between ISSHL and depression. The presence of the former induces or further exacerbates the latter, whereas a similar situation does not exist when the latter is an influencing factor.

Metacognitive biases have been repeatedly associated with transdiagnostic psychiatric dimensions of \'anxious-depression\' and \'compulsivity and intrusive thought\', cross-sectionally. To progress our understanding of the underlying neurocognitive mechanisms, new methods are required to measure metacognition remotely, within individuals over time. We developed a gamified smartphone task designed to measure visuo-perceptual metacognitive (confidence) bias and investigated its psychometric properties across two studies (N = 3410 unpaid citizen scientists, N = 52 paid participants). We assessed convergent validity, split-half and test-retest reliability, and identified the minimum number of trials required to capture its clinical correlates. Convergent validity of metacognitive bias was moderate (r(50) = 0.64, p < 0.001) and it demonstrated excellent split-half reliability (r(50) = 0.91, p < 0.001). Anxious-depression was associated with decreased confidence (β =  - 0.23, SE = 0.02, p < 0.001), while compulsivity and intrusive thought was associated with greater confidence (β = 0.07, SE = 0.02, p < 0.001). The associations between metacognitive biases and transdiagnostic psychiatry dimensions are evident in as few as 40 trials. Metacognitive biases in decision-making are stable within and across sessions, exhibiting very high test-retest reliability for the 100-trial (ICC = 0.86, N = 110) and 40-trial (ICC = 0.86, N = 120) versions of Meta Mind. Hybrid \'self-report cognition\' tasks may be one way to bridge the recently discussed reliability gap in computational psychiatry.

Researchers are interested in drug repurposing or drug repositioning of existing pharmaceuticals because of rising costs and slower rates of new medication development. Other investigations that authorized these treatments used data from experimental research and off-label drug use. More research into the causes of depression could lead to more effective pharmaceutical repurposing efforts. In addition to the loss of neurotransmitters like serotonin and adrenaline, inflammation, inadequate blood flow, and neurotoxins are now thought to be plausible mechanisms. Because of these other mechanisms, repurposing drugs has resulted for treatment-resistant depression. This chapter focuses on therapeutic alternatives and their effectiveness in drug repositioning. Atypical antipsychotics, central nervous system stimulants, and neurotransmitter antagonists have investigated for possible repurposing. Nonetheless, extensive research is required to ensure their formulation, effectiveness, and regulatory compliance.

OBJECTIVE: This study aimed to analyze the associations between rheumatoid arthritis (RA) and all-cause mortality and cardiovascular disease (CVD)-related mortality using data from the National Health and Nutrition Examination Survey (NHANES) and examine the potential mediating role of depression in these correlations.
METHODS: 19,165 participants across five NHANES cycles from 2007 to 2016 participated in this study. Multifactorial Cox regression models between RA, depression and two mortality outcomes and multifactorial regression models between RA and depression were constructed to examine their associations. The mediating role of depression has also been investigated.
RESULTS: The prevalence of RA in this study was 6.57 %, the all-cause mortality of RA patients was 20.57 %, and the CVD-related mortality was 6.12 %. In the fully adjusted model, RA was associated with all-cause mortality [hazard ratio (HR) = 1.28, 95 % confidence interval (CI) = 1.12 to 1.48] and CVD-related mortality (HR = 1.33, 95 % CI = 1.03 to 1.72), without detectable interaction among subgroups (P for interaction >0.05). RA also had a positive correlation with depression. Depression score demonstrated pronounced mediating effects in the connections between RA and two types of mortality, with mediation ratios of 18.2 % and 18.9 %.
CONCLUSIONS: The diagnosis of RA is self-reported and may be subject to recall bias.
CONCLUSIONS: RA was positively correlated with the risk of all-cause mortality and CVD-related mortality. Depression partially mediates these associations. Close attention to and active improvement of mental health in RA patients will be critical to decrease all-cause mortality and CVD-related mortality.

BACKGROUND: Heart rate variability (HRV) is often reduced in patients with major depressive disorder (MDD) and is linked to symptoms. However, prior studies have mainly focused on short-term HRV, with limited exploration of the 24-h HRV circadian rhythm, despite its ability to comprehensively capture overall HRV distribution and dynamic fluctuations. In this study, we investigated the circadian rhythms of 24-h HRV indices in patients with MDD and their associations with symptom severity.
METHODS: We recorded 24-h electrocardiograms in 73 patients with MDD (53 in major depressive episode and 20 in remission period) and 31 healthy controls. An extended cosine model was used to model the circadian rhythm of six HRV indices by five parameters: the mesor, amplitude, duty cycle, curve smoothness, and acrophase. Symptom severity was evaluated using the Hamilton Depression Scale and Hamilton Anxiety Scale.
RESULTS: Compared with the control group, patients with MDD had a significantly smaller SampEn mesor, higher HF duty cycle, and lower heart rate (HR) duty cycle. They also had a significantly higher curve smoothness for HR, RMSSD, and HF. The mesor for SampEn, along with the curve smoothness for HR and ln RMSSD, were associated with certain symptoms in patients with MDD.
CONCLUSIONS: The cross-sectional design and psychiatric treatment of most patients with MDD limited our findings.
CONCLUSIONS: Patients with MDD exhibit abnormal HRV circadian rhythms that are associated with symptoms. Moreover, 24-h ECG monitoring may potentially serve as an adjunct value to objectively evaluate clinical symptoms in these patients.

BACKGROUND: The mechanisms linking neural and behavioral indices of reduced reward sensitivity in depression, particularly in children, remain unclear. Reward positivity (RewP), a neural index of reward processing, has been consistently associated with depression. Separately, recent studies using the drift-diffusion model (DDM) on behavioral data have delineated computational indices of reward sensitivity. Therefore, the present study examined whether RewP is a neural mediator of DDM-based indices of reward processing in predicting pediatric depression across varying levels of symptom severity.
METHODS: A community sample of 166 girls, aged 8 to 14 years, completed two tasks. The first was a reward guessing task from which RewP was computed using electroencephalography; the second was a probabilistic reward-based decision-making task. On this second task, DDM analysis was applied to behavioral data to quantify the efficiency of accumulating reward-related evidence (drift rate) and potential baseline bias (starting point) towards the differently rewarded choices. Depression severity was measured using the self-report Children\'s Depression Inventory (CDI).
RESULTS: RewP was correlated with drift rate, but not starting point bias, towards the more rewarded choice. Furthermore, RewP completely mediated the association between a slower drift rate towards the more rewarded option and higher depression symptom severity.
CONCLUSIONS: Our findings suggest that reduced neural sensitivity to reward feedback might be a neural mechanism underscoring behavioral insensitivity to reward in children and adolescents with higher depression symptom severity, offering novel insights into the relationship between neural and computational indices of reward processing in this context.

Stressful life event is closely associated with depression, thus strategies that blunt or prevent the negative effect stress on the brain might benefits for the treatment of depression. Although previous study showed the role of protein kinase R (PKR)-like ER kinase (PERK) in inflammation related depression, its involvement in the neuropathology of chronic stress induced depression is still unknown. We tried to explore whether block the PERK pathway would alleviate the animals\' depression-like behavior induced by chronic restraint stress (CRS) and investigate the underlying mechanism. The CRS-exposed mice exhibited depression-like behavior, including anhedonia in the sucrose preference test (SPT), and increased immobility time in tail suspension test (TST) and forced swim test (FST). ISRIB administration for 2 weeks significantly improved the depression-like behavior in male mice exposed to CRS,which was manifested by markedly increasing the sucrose preference and reducing the immobility time in the FST and TST. However, we observed that exposure to the same dose of ISRIB in CRS female mice only showed improved anhedonia-like deficits,leaving un-altered improvement in the FST and TST. Mechanically, we found thatISRIB reversed the hypothalamic-pituitary-adrenal (HPA) axis hyperactivity, indicatingby decreased levels of serum corticosterone, reduced hippocampal glucocorticoidreceptor (GR) expression and expression of FosB in hypothalamic paraventricularnucleus (PVN), which was accompanied by preserved hippocampal neurogenesis. Thepresent findings further expand the potential role of ER stress in depression andprovide important details for a therapeutic path forward for PERK inhibitors in mood disorders.

Aims/Background Trait emotional intelligence is associated with anxiety and depression symptoms and quality of life in cancer patients. However, studies on the relationship of trait emotional intelligence with anxiety, depression, and quality of life in gastric cancer patients are limited. This study investigates the relationship of trait emotional intelligence with depression and quality of life in gastric cancer patients to provide a theoretical basis for clinical management. Methods A total of 270 patients with gastric cancer treated in our hospital from July 2020 to July 2023 were selected, of which 31 patients with missing questionnaire entries and missed visits were screened out, resulting in the enrolment of 239 gastric cancer patients in this study. In this survey, self-administered general information questionnaires, namely Trait Emotional Intelligence Short Form (TEIQue-SF), European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 (EORTC QLQ-C30), and Hospital Anxiety and Depression Scale (HADS) were used. Results TEIQue-SF total scores were positively correlated with QLQ-C30 scores (p < 0.001) and negatively correlated with HADS-A and HADS-D scores (p < 0.001). TEIQue-SF total score was a superior positive predictor of the QLQ-C30 score (β = 0.412, p < 0.001) and a superior negative predictor of the HADS score (β = -0.740, p < 0.001). TEIQue-SF total score (β = 0.141, p = 0.006) and HADS score (β = -0.665, p < 0.001) were good predictors of QLQ-C30 score. The direct effect of TEIQue-SF total score on QLQ-C30 score was 0.141, while HADS score between TEIQue-SF total score and QLQ-C30 score had a mediated effect value of 0.492. Conclusion Trait emotional intelligence not only directly affects the quality of life, but also indirectly affects the quality of life through anxiety and depression. Clinicians should pay attention to the anxiety, depression, and emotional intelligence of patients with gastric cancer to help them improve their quality of life.

BACKGROUND: Since the pathogenesis of depression is complex, antidepressant therapy remains unsatisfactory. Recent evidence suggests a link between depression and lipid metabolism. Saikosaponin (SS) exhibits antidepression and lipid-regulating effects in modern pharmacology. However, it is unknown whether lipid regulation is the key mechanism of the SS antidepressant effect and how it works.
OBJECTIVE: In this study, we investigated the relationship between the antidepressant activity of SS and the regulation of lipid metabolism and explored potential mechanisms.
METHODS: APOE-/- mice, in combination with the chronic unpredictable mild stress (CUMS) model, were used to study the relationship between SS antidepressant activity and lipid metabolism through behavioral, electrophysiological techniques, and non-targeted lipidomics. Western blot, primary cell culture technology, and laser speckle cerebral blood flow imaging were employed to elucidate potential mechanisms. GraphPad Prism was used for statistical analysis, and p < 0.05 was considered statistically significant.
RESULTS: APOE-/- mice exhibit more severe depressive-like behavior and dysregulation of sphingolipid metabolism in CUMS. SS alleviates depressive behavior and cortical sphingolipid metabolism disorder caused by CUMS, but has no effect on APOE-/- mice. SS alleviates the imbalance between ceramide (Cer) and sphingomyelin (SM) through acidic sphingomyelinase (AMSase). In addition, SS regulates neuronal glutamate release via sphingolipid metabolism, thereby alleviating the CUMS-induced inhibition of neurovascular coupling (regulates metabotropic glutamate receptor and IP3 receptor), which ameliorates the reduction of cerebral blood flow in depressed mice.
CONCLUSIONS: Our study highlights the role of lipid metabolism in the antidepressant activity of SS and explores its underlying mechanisms. This study provided new insights into the better understanding of the antidepressant mechanisms of phytomedicine while increasing the possibility of lipid metabolism as a therapeutic strategy for depression.