Reviews on the determinants of depression have been conducted, but they either focus exclusively on a particular set of determinants (ex. Remarkably, the authors concluded that children in inpatient settings were more likely to be non-suppressors than children in outpatient settings, which reflects adult findings of greater HPA-axis dysregulation associated with more severe depressive symptomatology [26]. https://doi.org/10.1016/j.biopsych.2019.08.016, Enko D, Brandmayr W, Halwachs-Baumann G, Schnedl WJ, Meinitzer A, Kriegshuser G (2018) Prospective plasma lipid profiling in individuals with and without depression. However, the roles of genetic polymorphisms in the dopaminergic pathway in adolescent depression have not been summarized. Abnormal hippocampal BDNF and miR-16 expression is associated with depression-like behaviors induced by stress during early life. investigated the blood levels of the same cytokines (TNF-, IL-1, and IL-6) in the group of treatment nave depressed adolescents and reported significantly increased IL-6 in the studied group when compared with healthy controls [55]. It is also engaged in neuroplastic processes in the adult brain. Front Behav Neurosci 9:329. https://doi.org/10.3389/fnbeh.2015.00329, Caspi A, Sugden K, Moffitt TE, Taylor A, Craig IW, Harrington H et al (2003) Influence of life stress on depression: moderation by a polymorphism in the 5-HTT gene. Oppenheimer C. W., Hankin B. L., Young J. F., Smolen A. https://doi.org/10.1017/S0954579417001407, Efstathopoulos P, Andersson F, Melas PA, Yang LL, Villaescusa JC, Regg J et al (2018) NR3C1 hypermethylation in depressed and bullied adolescents. Neurochem Int 51(5):246253. found that environmental stress during adolescence was associated with an increase in methylation of the proximal promoter of the SLC6A4 gene, which predicted increases in threat-related amygdala reactivity and a later manifestation of depressive symptoms [25]. Various methodological approaches (analysis of candidate genes, genome-wide association analysis, genome-wide sequencing) have been used, and a large number of the associations between genes and different clinical DD variants and DD subphenotypes have been published. The Role of Genetics In Depression As far as researchers know, it's the interplay of genes and other factors (such as environment and trauma) that determine A significant problem in finding an effective treatment for childhood and adolescent depression is that antidepressants were first developed for adults, and they do not necessarily have efficacy in the youth population [7]. Such correlation has also been confirmed in the study performed on adolescent patients [45]. Although s allele seems conducive to the development of depression in adolescence, studies show no relation between the 5-HTTLPR polymorphism and depression severity once it occurs [18]. BDNF genotype moderates the relation between physical activity and depressive symptoms. The most commonly examined polymorphism was the 5-HTTLPR variable number tandem repeat (VNTR), which consists of the s/s, s/l, and l/l genotypes. (2012) study showed that no significant increase in suicide-related outcomes was observed in children and adolescents after using individual SSRIs, such as paroxetine, fluoxetine, sertraline, citalopram, and escitalopram. https://doi.org/10.1523/JNEUROSCI.5158-04.2005, Pea CJ, Kronman HG, Walker DM, Cates HM, Bagot RC, Purushothaman I et al (2017) Early life stress confers lifelong stress susceptibility in mice via ventral tegmental area OTX2. J Child Adolesc Psychopharmacol 23(2):117122. Mata J., Thompson R. J., Gotlib I. H. (2010). Although the authors did not find any direct relationship between the BDNF Val66Met polymorphism and a depressive symptom score, the BDNF Val allele enhanced a depressive response to stress. FKBP51 is a potent inhibitor of the glucocorticoid receptor, and thus, an essential regulator of the HPA-axis stress response. Biol Psychiatry 59(8):673680. Some studies investigated the threeway interaction model of BDNF Val66Met polymorphism, the serotonin transporter linked promoter region (5-HTTLPR) polymorphism, and childhood adversity in predicting the development of depression. Long-lasting depression with moderate or severe intensity is a serious medical condition that can lead to suicide. This study updated the genetic findings in adolescent depression with an age range of 1019 years defined by WHO as adolescence and 2025 years as young adult. Int Rev Neurobiol 119:373393. Approximately 92.3% (24/26) of studies for the association between 5-HTTLPR polymorphism and depression in adolescents yielded a positive outcome (Table (Table2).2). Considering the essential part that 5-HTT plays in pharmacotherapy, it is not surprising that 5-HTTLPR polymorphism has also been widely investigated as a potential predictor of antidepressant treatment response. suggested a role of altered MET expression in the pathogenesis of depression among adolescents [116]. Most studies did not include age or gender-matched control individuals. reported that higher SLC6A4 promoter methylation status was significantly associated with adverse life events as well as worse clinical presentation of depression, and they suggested that SLC6A4 methylation status could serve as a marker for childhood adversities and as a clinical biomarker for specific presentations of depression [24]. J Psychiatr Res 114:110. https://doi.org/10.1016/j.jpsychires.2017.03.015, Szczepankiewicz A, Leszczyska-Rodziewicz A, Pawlak J, Narozna B, Rajewska-Rager A, Wilkosc M et al (2014) FKBP5 polymorphism is associated with major depression but not with bipolar disorder. For instance, the levels of total cholesterol (TCH) and low-density lipoproteins (LDL) have been shown to be both increased and decreased in depression [94,95,96]. [19]. Psychoneuroendocrinology 56:4551. J Affect Disord 150(2):415423. Careers, Unable to load your collection due to an error. Since early-onset episodes of depression have been associated with a worse prognosis of the future disease course, early successful treatment response is among the highest priorities for improving mental health [6]. WebWhich genetic indicators play a role in increasing the risk of adolescent depression? The study revealed the vitamin B12 levels to be significantly lower and the homocysteine levels to be remarkably higher in a group of depressed children. Although there is strong evidence proving that the expression of FKBP5 modulates the response to antidepressants in adults [46, 47], no such correlation was found in the study performed on the group of adolescent patients [21]. Genetics of childhood and adolescent depression: insights into Based on the report from Hammen et al. J Child Adolesc Psychopharmacol 26(8):727732. Teen Depression Cattaneo A., Bocchio-Chiavetto L., Zanardini R., Milanesi E., Placentino A., Gennarelli M. (2010). For instance, a study by Tsuchimine et al. Consistently with these findings, the study on BDNF concentrations among children with ADHD symptomatology revealed no relationship between BDNF serum levels and depressive symptoms [87]. Selective serotonin reuptake inhibitors (SSRIs) are the first line treatment for depression in the clinic. This theory is supported by studies showing a decreased level of BDNF in the post-mortem brain samples of patients suffering from MDD [66]. https://doi.org/10.1016/s0006-3223(96)00470-2, Dorn LD, Burgess ES, Susman EJ, von Eye A, DeBellis MD, Gold PW et al (1996) Response to oCRH in depressed and nondepressed adolescents: does gender make a difference? Purinergic Signal 13(2):203214. SY: study design, data extraction, data analysis, critical revision of manuscript, and a guarantor of the review. According to the neuroinflammatory theory of depression, IL-6 and BDNF remain closely related, as chronic neuroinflammation is considered to cause a decrease of BDNF level in the brain [49]. Further research on this subject might contribute to inventing more personalized and more effective antidepressant treatment strategies in child and adolescent depression. FOIA Within the promoter of the serotonin transporter gene (SLC6A4), there is a serotonin-transporter-linked polymorphic region (5-HTTLPR) with a long (l) or short (s) allele resulting in respectively higher and lower SLC6A4 gene activity [8]. 3). The influence of family structure, the TPH2 G-703T and the 5-HTTLPR serotonergic genes upon affective problems in children aged 1014 years. https://doi.org/10.1016/s0006-3223(03)00181-1, Molendijk ML, Bus BA, Spinhoven P, Penninx BW, Kenis G, Prickaerts J et al (2011) Serum levels of brain-derived neurotrophic factor in major depressive disorder: state-trait issues, clinical features and pharmacological treatment. Brent D., Melhem N., Ferrell R., Emslie G., Wagner K. D., Ryan N., et al.. (2010). Starr L. R., Hammen C., Brennan P. A., Najman J. M. (2013). 5-HTT (5-HTTLPR polymorphism) is the most frequently examined gene (26 articles) followed by Brain-derived neurotropic factor (BNDF; 12 articles). Department of Child and Adolescent Psychiatry, Poznan University of Medical Sciences, Szpitalna St. 27/33, 60-572, Poznan, Poland, Department of Psychiatric Genetics, Medical Biology Center, Poznan University of Medical Sciences, Rokietnicka St. 8, 60-806, Poznan, Poland, You can also search for this author in Adolescents carrying a missense mutation in the CART gene exhibit increased anxiety and depression. Depression persistence and serotonin transporter genotype in adolescents under usual care conditions. Based on the potential effects of caffeine on depressive symptoms, the role of adenosine receptors in depression has been hypothesized [110]. Vitamin B12 and B6 are also crucial to clear homocysteine by transsulfuration into glutathione. Biol Psychiatry 42(8):669679. More studies on the youth population are needed to verify whether such metabolic disturbances may underlie the resistance towards antidepressant treatments, at least in some cases. Jiang X., Xu K., Hoberman J., Tian F., Marko A. J., Waheed J. F., et al.. (2005). The end date for the search is August 29, 2015. Depression is a common disorder affecting an estimated 350 million people worldwide. Some proved that the Met allele was associated with an increased likelihood of MDD in adolescent females through effects on amygdala-cortical connectivity [70]. https://doi.org/10.1016/j.bbi.2015.06.001, Goldsmith DR, Rapaport MH, Miller BJ (2016) A meta-analysis of blood cytokine network alterations in psychiatric patients: comparisons between schizophrenia, bipolar disorder and depression. Another attitude to explore the relation between genetics, environmental adversity and depression is through epigenetic modifications in stress-related genes. Goodyer I. M., Croudace T., Dudbridge F., Ban M., Herbert J. Nobile M., Rusconi M., Bellina M., Marino C., Giorda R., Carlet O., et al.. (2009). More studies, however, are needed to confirm this hypothesis. revealed no influence of 5-HTTLPR or TPH1 polymorphism on antidepressant response in the group of treatment resistant depressed adolescents [21]. Increased serum lipids are often associated with obesity, which has been associated with depressive symptoms in the pediatric population [99]. The authors found that higher methylation levels within the MET gene were associated with higher depression scores and susceptibility for suicidal symptoms in the population of adolescents.
Noida To Roorkee Distance, Lake Forest School District 2023-2024 Calendar, Mt Carmel Basketball Coach, Snooky's On The Water Menu, Follow The Money South Pole, Articles W