Major depression disorder (MDD) is a complex and chronic disease that ranks fourth as cause of disability worldwide. About 14 million adults in the USA are believed to have MDD, and an estimated 75 % attempt suicide making MDD a major public health problem. Neuroticism has been recognized as an endophenotype of MDD; however, few genome-wide association (GWA) analyses of neuroticism as a quantitative trait have been reported to date. The aim of this study is to identify genome-wide genetic variants affecting neuroticism using a European sample. A linear regression model was used to analyze the association with neuroticism as a continuous trait in the Netherlands Study of Depression and Anxiety and Netherlands Twin Registry population-based sample of 2,748 individuals with Perlegen 600K single nucleotide polymorphisms (SNPs). In addition, the neuroticism-associated genes/loci of the top 20 SNPs (p < 10-4) were examined with anti-social personality disorder (ASPD) in an Australian twin family study. Through GWA analysis, 32 neuroticism-associated SNPs (p < 10-4) were identified. The most significant association was observed with SNP rs4806846 within the TMPRSS9 gene (p = 7.79 × 10-6) at 19p13.3. The next best signal was in GRIN2B gene (rs220549, p = 1.05 × 10-5) at 12p12. In addition, several SNPs within GRIN2B showed borderline associations with ASPD in the Australian sample. In conclusion, these results provide a possible genetic basis for the association with neuroticism. Our findings provide a basis for replication in other populations to elucidate the potential role of these genetic variants in neuroticism and MDD along with a possible relationship between ASPD and neuroticism.

Major depression disorder (MDD) is a complex and chronic disease that ranks fourth as cause of disability worldwide. About 14 million adults in the USA are believed to have MDD, and an estimated 75 % attempt suicide making MDD a major public health problem. Neuroticism has been recognized as an endophenotype of MDD; however, few genome-wide association (GWA) analyses of neuroticism as a quantitative trait have been reported to date. The aim of this study is to identify genome-wide genetic variants affecting neuroticism using a European sample. A linear regression model was used to analyze the association with neuroticism as a continuous trait in the Netherlands Study of Depression and Anxiety and Netherlands Twin Registry population-based sample of 2,748 individuals with Perlegen 600K single nucleotide polymorphisms (SNPs). In addition, the neuroticism-associated genes/loci of the top 20 SNPs (p < 10-4) were examined with anti-social personality disorder (ASPD) in an Australian twin family study. Through GWA analysis, 32 neuroticism-associated SNPs (p < 10-4) were identified. The most significant association was observed with SNP rs4806846 within the TMPRSS9 gene (p = 7.79 × 10-6) at 19p13.3. The next best signal was in GRIN2B gene (rs220549, p = 1.05 × 10-5) at 12p12. In addition, several SNPs within GRIN2B showed borderline associations with ASPD in the Australian sample. In conclusion, these results provide a possible genetic basis for the association with neuroticism. Our findings provide a basis for replication in other populations to elucidate the potential role of these genetic variants in neuroticism and MDD along with a possible relationship between ASPD and neuroticism.

Background: Major depressive disorder (MDD) is a universally prevalent, genetic, and environment dependent mental condition that disables people of every culture, race, gender, and age. While the gender differences for MDD have been widely reported in literature, few genome-wide analyses of gender differences have been reported to date. Methods: We conducted a genome-wide association analysis of gender differences for MDD using the Netherlands NESDA and NTR population-based samples (1726 cases and 1630 controls). PLINK software was used to analyze the genome-wide association data of Perlegen 600 K SNP Chips. Results: We identified 40 male-specific and 56 female-specific MDD associated SNPs with P-values less than 10- 4. The best male-specific SNP was rs9352774 (P = 2.26 × 10- 6) within LGSN gene while the best female-specific SNP was rs2715148 (P = 5.64 × 10- 7) within PCLO gene. We also found 38 SNPs showing gene × gender interactions in influencing MDD (P < 10- 4). The best SNP was rs12692709 (P = 5.75 × 10- 6) near FIGN gene at 2q24.3 while the next best SNP was rs11039588 (P = 1.16 × 10- 5) within OR4B1 gene. Limitations: The findings from this study need be replicated in other populations. Conclusions: These results provide genetic basis for gender differences in MDD and will serve as a resource for replication in other populations to elucidate the potential role of these genetic variants in MDD.

Purpose: The study examined the associations of multiple psychiatric and chronic conditions with the self-reported history of major depressive disorder (MDD) among patients with opioid use disorder (OUD) and tested whether the associations differed by gender. Methods: We conducted a secondary data analysis of baseline data from a clinical trial including 1,646 participants with OUD, of which 465 had MDD. A variable cluster analysis was used to classify chronic medical and psychiatric conditions. Multivariable logistic regression analyses were used to estimate their associations with MDD in subjects with OUD. Results: Nine variables were divided into three clusters: cluster 1 included heart condition, hypertension, and liver problems; cluster 2 included gastrointestinal (GI) problems and head injury, and cluster 3 included anxiety disorder, bipolar disorder, and schizophrenia. The overall prevalence of MDD in participants with OUD was 28.3% (22.8% for males and 39.5% for females). Gender, anxiety disorder, schizophrenia, liver problems, heart condition, GI problems, and head injury were significantly associated with MDD. Gender-stratified analyses showed that bipolar disorder, liver problems and individuals with one chronic condition were associated with MDD only in males, whereas heart condition, hypertension, and GI problems were associated with MDD only in females. In addition, anxiety disorder, head injury, individuals with one or more than two psychiatric conditions, and individuals with more than two chronic conditions were associated with MDD regardless of gender. Conclusions: Treatment plans in patients with OUD should not only address MDD but also co-morbid psychiatric and chronic medical conditions that occur with MDD.

Ammonia is a toxic by-product of protein catabolism and is involved in changes in glutamate metabolism. Therefore, ammonia metabolism genes may link a range of diseases involving glutamate signaling such as Alzheimer’s disease (AD), major depressive disorder (MDD), and type 2 diabetes (T2D). We analyzed data from a National Institute on Aging study with a family-based design to determine if 45 single nucleotide polymorphisms (SNPs) in glutaminase (GLS), carbamoyl phosphate synthetase 1 (CPS1), or glutamate-ammonia ligase (GLUL) genes were associated with AD, MDD, or T2D using PLINK software. HAPLOVIEW software was used to calculate linkage disequilibrium measures for the SNPs. Next, we analyzed the associated variations for potential effects on transcriptional control sites to identify possible functional effects of the SNPs. Of the SNPs that passed the quality control tests, four SNPs in the GLS gene were significantly associated with AD, two SNPs in the GLS gene were associated with T2D, and one SNP in the GLUL gene and three SNPs in the CPS1 gene were associated with MDD before Bonferroni correction. The in silico bioinformatic analysis suggested probable functional roles for six associated SNPs. Glutamate signaling pathways have been implicated in all these diseases, and other studies have detected similar brain pathologies such as cortical thinning in AD, MDD, and T2D. Taken together, these data potentially link GLS with AD, GLS with T2D, and CPS1 and GLUL with MDD and stimulate the generation of testable hypotheses that may help explain the molecular basis of pathologies shared by these disorders.

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Abstract Introduction and Background Many people in the pediatric population are be brushed off and misdiagnosed when it comes to depression. I decided to research into pediatric depression and how the effects of their peers, parents, and exposure to violence correspond with depression and how it effects their daily life. Purpose Statement The purpose of this literature review is to systematically and critically appraise current literature to examine the associations between pediatric depression and sleep issues, exposure to violence, peer relationships, and parental criticism. Literature Review For this literature review I gathered a total of 5 articles which are included in this review. All the 5 articles are academic journals. These articles all come from CINAHL complete from the ETSU library database. Findings When the pediatric population is exposed to emotional abuse, emotional neglect, physical abuse, physical neglect, peer victimization and peer fighting, they were reported to have significantly greater depressive symptoms and hopelessness than the pediatric population who did not experience as much violence and neglect (Benton et al. 2020). Children who had preschool-onset major depressive disorder, after receiving parent-child interactive therapy with a focus on emotional development were found to experience a significant reduction in insomnia, daytime fatigue, and total sleeping problems (Hoyniak et al., 2020). There was also a strong correlation that the more parental criticism an adolescence receives, the higher the risk for major depression there is (Nelemans et al., 2020). The CLPM model indicated that depressive symptoms increased the risk for subsequent peer rejection consistently and peer acceptance mainly before eighth grade (Yang et al., 2020). And in the patients who came to the ER with non-psychiatric complaints, after screening for depression many of their results indicated a moderately-severe depression score which presents a need for additional help from a mental health care provider (Arrojo and Hooshmand, 2021). Conclusions Overall, there is a strong correlation between pediatric depression and sleep issues, exposure to violence, peer relationships, and parental criticism. The studies proved that the more parental criticism a child received, the more depressive symptoms they faced, as well as the more sleeping issues they experienced. The data also proved that in adolescence the influence of peers is strong and peer relationships have heavy influence on the depressive symptoms shown by adolescence. When children are exposed to a ‘web of violence’ they are also more inclined to experience depression and many children try to internalize their mental health issues to please their parents. There needs to be more general education about pediatric depression and more implementations of mandatory screenings added to the EHR. For many of these studies, if they were to be performed again, they would benefit from more diversity as well as larger sample sizes. This would provide a more generalizable set of data that could be applied in more places.

Major depressive disorder (MDD) is rapidly growing and one of the most common causes of disability and mortality worldwide. People with MDD often display brain changes such as adisrupted balance in neurotransmitters, impaired neurogenesis and neuroplasticity. Traditionally has MDD been treated with medications and talking therapies (psychotherapy). Studies have shown that just around 50 % of people with MDD get improvements from common traditional treatments.Therefore is there a great need for a better understanding of MDD and new treatments. There is now an emerging field of research that indicates that the gut microbiota plays a crucial role in disturbing normal brain functioning in MDD. This connection between the gut and the brain is called the gutbrain axis.The thesis aims to investigate if there is a connection between gut microbiota disruption and MDD and if gut microbiota restoration can be a potential effective future treatment for MDD. Key findings of the thesis were, studies show that people with MDD often display gut microbiota disruption and chronic low grade inflammation. Studies also indicate that this inflammation can cause the specific brain change often displayed in people with MDD. One of the most critical findings in the thesis was that gut brain treatments affect tryptophan metabolism, which affects the risk of MDD. The research area of the gut brain axis is still new and many more studies are needed,particularly in humans.

Background: Major depressive disorder is one of the leading diseases in the world. While anti-depressive medication is the most commonly used treatment, studies shows conflicting results of its benefits, where other alternative treatments are getting more attention such as psychological treatment and physical activity. Aim: The study aimed to illuminate the meaning of physical activity for adult patients suffering from major depressive disorder. Method: The method used is a literature review of nine original scientific articles, published in Cinahl, PubMed and PsycArticles databases between 2010-2020, limited to peer-review and English language. Results: The result showed a decrease in depressive symptoms as shown in rating scales such as HDRS, BDI and MADRS, in patients treated with physical activity. Patients suffering from severe major depressive disorder showed paramount difference pre-post intervention, despite their initial state of disability. Conclusion: Regardless of the severity of disease, physical activity shows a valid effect as an adjunct treatment in adults suffering from major depressive disorder. The result shows that while the use of physical activity as therapy is warranted in patients with major depressive disorder, adherence to treatment is of outmost importance, and the support from health professionals is mandatory.

BACKGROUND: Major Depressive Disorder (MDD) is a common mental health illness, characterized by persistent feelings of sadness, diminished interests, guilt, low-self esteem, and disturbances in sleep and appetite. A significant percentage of patients with MDD are treatment resistant. Electroconvulsive Therapy (ECT) is a biological procedure utilized for treatment resistant illnesses. Diagnosis and clinical conditions primarily dictate when ECT is the appropriate treatment modality for an individual. Circumstances requiring rapid clinical response, risks affiliated with alternative treatments, resistance to pharmacotherapy, and medical history are all factors that designate ECT as the treatment of choice. METHODS: The objective of this systematic review was to examine how different anesthetics or combinations of agents affect ECT’s therapeutic efficacy in depressed, adult patients. Electroencephalography (EEG) and motor seizure durations and Hamilton Depression Rating Scale (HDRS) scores were used as primary measures of clinical outcomes. Two rounds of literature searches were conducted in the PubMed, Web of Science, and Google Scholar databases to identify randomized controlled trials and crossover trials that examined the effects of different intravenous sedatives and hypnotic agents on ECT. Two reviewers independently evaluated the internal validity and quality of studies, extracted data, and analyzed statistics. Utilizing all relevant data, standardized mean differences (SMD) with 95% confidence intervals (CIs), and heterogeneity measures were calculated. Ten studies with 373 participants were included. RESULTS: Thiopental only anesthesia was associated with longer EEG seizure duration when compared to propofol only treatment. The pooled effect size from studies with propofol anesthesia also suggests that this agent is associated with shorter seizure durations. If assessed individually with thiopental, the combination of ketamine and thiopental is correlated with increased motor as well as EEG seizure durations. When pooled; however, studies with patient groups assigned to anesthesia consisting of ketamine and another primary agent do not show significant differences either in EEG or motor seizure durations. Additionally, no difference exists in HDRS score reductions between propofol and methohexital. Of note; however, ketamine combined with either propofol or thiopental had significantly greater decreases in HDRS scores. CONCLUSION: Choice of anesthetic should be determined based on anticipated clinical outcome, adverse effect profile, reemergence, and patient preference. If long seizures are preferred, thiopental may be a reasonable option. However, if significantly larger decreases in depression score are preferred, then the combinations of ketamine and propofol or ketamine and thiopental appear to be the therapies of choice. Small sample sizes and insufficient clinical data limit the interpretations of these variables that determine therapeutic efficacy. Larger randomized control trials and crossover trials would provide greater insight into the optimal use of intravenous anesthetic agents with minimal adverse effects.