Relevant bibliographies by topics / Predisposition to depression

Academic literature on the topic 'Predisposition to depression'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Predisposition to depression"

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Sandler, M., Vivette Glover, and Patricia Hannah. "Postnatal depression: Predisposition and prediction." Journal of Obstetrics and Gynaecology 10, no. 3 (January 1990): 238–39. http://dx.doi.org/10.3109/01443619009151181.

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Beatson, Josephine, and Suzanna Taryan. "Predisposition to Depression: The Role of Attachment." Australian & New Zealand Journal of Psychiatry 37, no. 2 (April 2003): 219–25. http://dx.doi.org/10.1046/j.1440-1614.2003.01126.x.

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Objective: To examine the hypothesis that adverse early relational experiences causing activation of the hypophysial-pituitary-adrenal (HPA) axis during critical early stages of development can predispose to depression. Patients thus affected are likely to manifest insecure patterns of attachment in close relationships and are vulnerable to depression after adverse life events. Method: The literature pertaining to sensitization of the HPA axis in early life and the neurobiology of attachment is examined. Results: Adverse early relational experiences can result in activation of the HPA axis, causing sensitization of depression pathways in the brain. Secure attachment acts as a buffer against HPA activation in response to stress. Infants with insecure attachment lack this buffering effect and may be predisposed to depression and other psychiatric disorders in response to psychosocial stressors. Conclusions: There is a patient group predisposed to depression on the basis of adverse early life experience. In these cases, the neurobiology of attachment offers a means of integrating findings concerning sensitization of the HPA axis in infancy, the effects of early life experience on brain development, and predisposition to depression and other psychiatric disorders. These findings have important implications for the development of interventions aimed at prevention and treatment for this patient group.
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Knyazev, Gennady G., Andrey V. Bocharov, Alexander N. Savostyanov, and Jaroslav Slobodskoy-Plusnin. "Predisposition to depression and implicit emotion processing." Journal of Clinical and Experimental Neuropsychology 37, no. 7 (July 24, 2015): 701–9. http://dx.doi.org/10.1080/13803395.2015.1061483.

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Martin, Maryanne. "Neuroticism as predisposition toward depression: A cognitive mechanism." Personality and Individual Differences 6, no. 3 (January 1985): 353–65. http://dx.doi.org/10.1016/0191-8869(85)90060-1.

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McGuffin, Peter, and Randy Katz. "The Genetics of Depression and Manic-Depressive Disorder." British Journal of Psychiatry 155, no. 3 (September 1989): 294–304. http://dx.doi.org/10.1192/bjp.155.3.294.

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Depressive disorders are more common in the relatives of depressed probands than in the population at large, and there is compelling evidence that the familial aggregation of bipolar disorder and severe unipolar depression is at least partly due to genetic factors. However, the evidence concerning ‘non-endogenous' depression is less clear, and family environment probably plays a stronger role. Much current research is focused on two areas: firstly, the mode of inheritance of manic-depressive illness, with the use of molecular biological techniques to detect and localise major genes; and secondly, the ways in which familial predisposition and environmental insults combine to produce depressive disorder.
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Ferrier, I. N. "Comparisons of Clinical Efficacy." British Journal of Psychiatry 163, S20 (July 1993): 25–28. http://dx.doi.org/10.1192/s0007125000292337.

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This paper does not attempt to review the whole topic of clinical efficacy but will consider general concepts, particularly in the light of the advent of the serotonin (5-HT) uptake inhibitors (SSRIs).The aetiology of depression is complex. In most cases there is some form of predisposition based on problematical family dynamics, disordered family communication and/or genetic factors; each may be present to a variable extent. On top of this predisposition, some form of stimulus - ‘stress’, an external problem, loss of control, a physical disorder, adverse life circumstances - appears to affect those who are already primed. There are a variety of possible outcomes from this combination of predisposition and stimuli: low mood, depression in the full syndromic sense, and depression with biological features. It seems likely that, particularly with severe depressions (the major syndromic forms and those with biological features), there are neuroendocrine and neurochemical changes to mediate the effects of stress into those of the clinical symptoms and signs. It has been hypothesised that stressors induce adaptive neurochemical changes, failure of which may engender behavioural disturbances (Anisman & Zacharko, 1992). However, there are also many individuals who may not undergo this process, but who probably have some cognitive or learned change leading to dysphoria; this aspect needs to be considered carefully in relation to efficacy.
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Fatima, Rida, and Alishba Hania. "PREDISPOSITION OF EARLY MALADAPTIVE SCHEMAS AND POSTPARTUM DEPRESSION DURING COVID-19 CRISIS: MEDIATION OF MINDFULNESS." PSYCHIATRIA DANUBINA 34, no. 1 (April 22, 2022): 148–56. http://dx.doi.org/10.24869/psyd.2022.148.

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Shnayder, Natalia A., Maxim A. Novitsky, Nikolay G. Neznanov, Oleg V. Limankin, Azat R. Asadullin, Artem V. Petrov, Diana V. Dmitrenko, Ekaterina A. Narodova, Natalia V. Popenko, and Regina F. Nasyrova. "Genetic Predisposition to Schizophrenia and Depressive Disorder Comorbidity." Genes 13, no. 3 (March 2, 2022): 457. http://dx.doi.org/10.3390/genes13030457.

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Background: Patients with schizophrenia have an increased risk of depressive disorders compared to the general population. The comorbidity between schizophrenia and depression suggests a potential coincidence of the pathophysiology and/or genetic predictors of these mental disorders. The aim of this study was to review the potential genetic predictors of schizophrenia and depression comorbidity. Materials and Methods: We carried out research and analysis of publications in the databases PubMed, Springer, Wiley Online Library, Taylor & Francis Online, Science Direct, and eLIBRARY.RU using keywords and their combinations. The search depth was the last 10 years (2010–2020). Full-text original articles, reviews, meta-analyses, and clinical observations were analyzed. A total of 459 articles were found, of which 45 articles corresponding to the purpose of this study were analyzed in this topic review. Results: Overlap in the symptoms and genetic predictors between these disorders suggests that a common etiological mechanism may underlie the presentation of comorbid depression in schizophrenia. The molecular mechanisms linking schizophrenia and depression are polygenic. The most studied candidate genes are GRIN1, GPM6A, SEPTIN4, TPH1, TPH2, CACNA1C, CACNB2, and BCL9. Conclusion: Planning and conducting genome-wide and associative genetic studies of the comorbid conditions under consideration in psychiatry is important for the development of biological and clinical predictors and a personalized therapy strategy for schizophrenia. However, it should be recognized that the problems of predictive and personalized psychiatry in the diagnosis and treatment of schizophrenia and comorbid disorders are far from being resolved.
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Abkevich, Victor, Nicola J. Camp, Charles H. Hensel, Chris D. Neff, Deanna L. Russell, Dana C. Hughes, Agnes M. Plenk, et al. "Predisposition Locus for Major Depression at Chromosome 12q22-12q23.2." American Journal of Human Genetics 73, no. 6 (December 2003): 1271–81. http://dx.doi.org/10.1086/379978.

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Willner, P., and P. J. Mitchell. "The validity of animal models of predisposition to depression." Behavioural Pharmacology 13, no. 3 (May 2002): 169–88. http://dx.doi.org/10.1097/00008877-200205000-00001.

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Dissertations / Theses on the topic "Predisposition to depression"

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Woods, Lance Gregory 1945. "Sex-role attributes, self-perception and predisposition to depression in early adolescence." Diss., The University of Arizona, 1998. http://hdl.handle.net/10150/288838.

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This study investigated the relationship of sex-role attributes, self-perception, and predisposition to depression in early adolescence. 235 students from middle schools in Dade County, Florida were asked to complete three instruments; the Personal Attributes Questionnaire, the Perceived Competence Scale, and the Children's Depression Inventory. The study was designed to determine the effects of sex-role attributes on self-perception and predisposition to depression in early adolescence. More specifically, the study asked whether instrumental attributes were implicated in higher levels of perceived competence and lower depressive symptomatology while the reverse was true for those with expressive attributes. The results of the study confirmed that instrumentality and perceived competence appear to inoculate against depression. Instrumentality for the entire sample was, in fact, significantly correlated with higher overall perceived competence and significantly inversely correlated with depressive symptomatology. Contrary to the initial hypotheses, however, expressive traits were also positively correlated with higher perceived competence and lower levels of depressive symptomatology in the entire sample. Within the sample, though, those designated as expressive individuals did report a positive but nonsignificant relationship between expressive traits and increased depression measures. Instrumental males and androgynous females reported the lowest percentages of elevated depression scores while undifferentiated males and females reported the highest percentage. While both perceived competence and instrumental attributes were found to have a significant inverse relationship with depression, the hypothesis that instrumental traits mediated the relationship between perceived competence and depression was not borne out with both perceived competence and instrumentality maintaining significant contributions to overall levels of depressive symptoms. The same was not true for expressive attributes as they related to the mediation of perceived competence and depression. When both perceived competence and expressivity were considered expressivity failed to maintain a significant relationship with levels of depressive symptoms. The study also reflected sex role attributes as coping styles similar to problem focused and emotion focused approaches and also suggested an awareness that a coping style other than the individual's predominant style seemed to exist.
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Majumder, Irina. "Antidepressant-like effects of 3,4-methylenedioxymethamphetamine (MDMA, ecstasy)." Thesis, 2010. http://hdl.handle.net/2440/62483.

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3,4-methylenedioxymethamphetamine (MDMA, ecstasy) is a popular club drug that is abused worldwide. The main subjective effects of the drug include enhanced mood and self-esteem. Due to these effects, ecstasy may be used at higher rates by people with pre-existing mood disorders, or a predisposition to depression, in order to ‘self-medicate’ their state. This, in turn, may lead to more regular drug use, and, hence, a higher risk of side effects and negative impact on health. Moreover, some mechanisms of MDMA action in the brain are similar to those of clinically prescribed antidepressants, as the drug primarily affects the serotonin (5-HT) system. This suggests that the drug may have antidepressant‐like activity. The studies reported here, both preclinical and clinical, were designed to investigate possible antidepressant-like effects of MDMA in subjects with a predisposition to depression. In the animal study, the effects of MDMA following single and repeated administration were compared between Sprague-Dawley and the Flinders Sensitive Line rat strains, the latter being a putative model of depression. The drug’s effects on behaviour were assessed in the Forced Swimming Test, which is widely used to detect the depressivelike state in laboratory animals. Acute MDMA administration had a dose-dependent antidepressant-like effect that was more evident in the Flinders Sensitive Line animals. This effect was diminished following 3 weeks of repeated drug injection, possibly due to the development of tolerance. The chosen dosing regime didn’t affect the cortical levels of 5-HT and its metabolite. 40 current ecstasy users participated in the clinical study. Predisposition to depression was assessed using a questionnaire (Brief Symptom Inventory) that determines the rates of distress in various psychological spheres. Mood scores and depressive symptoms were assessed when participants were drug-free and when they attended a social gathering. Twenty participants, with and without a predisposition to depression, who voluntarily chose to take a pill at a social gathering, were assessed 1 hour after drug consumption, and the mood disturbance and depressive symptoms were compared with participants who abstained from pill consumption. Ecstasy users with a predisposition to depression reported higher mood disturbance and more prominent depressive symptoms when they were not under the influence of the drug. At the party, mood was improved in all participants irrespective of whether they chose to consume a pill, whereas subjects predisposed to depression reported a relative decrease in depressive symptoms only after pill consumption, which may be considered as an antidepressant‐like effect of the drug. Certain variants of the 5-HT transporter gene polymorphism were associated with higher depressive scores. Analysis of the effects of different previous ecstasy exposure revealed that subjects with a greater number of pills consumed in their lifetime report more prominent positive effects following ecstasy consumption, which may explain their more frequent use. In sum, an immediate antidepressant-like effect of MDMA was evident both in an animal model of depression and in users predisposed to depression. This may suggest the self-medicating potential of MDMA in subjects with a predisposition to depression.
Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 2010
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Books on the topic "Predisposition to depression"

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Ismail, Khalida, Andreas Barthel, Stefan R. Bornstein, and Julio Licinio, eds. Depression and Type 2 Diabetes. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198789284.001.0001.

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Type 2 diabetes is predicted to affect between 10% and 25% of the world population in the next 20 years. Depression is a common comorbid condition in those affected with type 2 diabetes, and the combination of these conditions is associated with a poorer prognosis, including earlier mortality. Genetic and epigenetic predisposition and overlap of risk factors related to our modern lifestyle seem to drive the shared biology of diabetes and depression. This book aims to provide an understanding of the sequelae of events leading to the frequent comorbidity of diabetes and depression. This book project has been supported by the transCampus of Kings College London and Technical University of Dresden. Chapter by chapter, internationally recognized clinicians and scientists have summarized the state of the art and outstanding controversies of the epidemiology, mechanisms, and treatment of the depression–type 2 diabetes comorbidity. This book is relevant for all health professionals including the general practitioner and specialist clinicians in internal medicine, endocrinology, diabetes and metabolic diseases, neurology, psychiatry, and psychology as well as students interested in this topic.
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Keel, Pamela K., and Lauren A. Holland. Eating Disorders. Edited by C. Steven Richards and Michael W. O'Hara. Oxford University Press, 2014. http://dx.doi.org/10.1093/oxfordhb/9780199797004.013.017.

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This chapter examines patterns of comorbidity between eating disorders and mood, anxiety, and substance use disorders along with evidence regarding support for different theoretical models that may account for these patterns. Although comorbidity estimates may be inflated by reliance on treatment-seeking samples and double counting of symptoms that overlap between syndromes, evidence supports elevated risk of mood, anxiety, and substance use disorders in anorexia nervosa, bulimia nervosa, and binge eating disorder. Data from family and twin studies support that eating and anxiety disorders may have a shared diathesis, consistent with the common cause model. Data from longitudinal studies suggest that eating disorders may increase vulnerability for developing a substance use disorder, consistent with the predisposition model. In contrast, comorbidity between eating and mood disorders, such as depression, remains poorly understood. Clinical issues regarding comorbidity of depression and eating disorders along with guidelines for clinicians treating patients with comorbid depression and eating disorders are discussed.
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Hand-Me-Down Genes and Second-Hand Emotions: Overcome the Genetic and Environmental Predispositions That Control Your Life. Thomas Nelson Inc, 1993.

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Bengesser, Susanne, and Eva Reininghaus. Genetics of Bipolar Disorder. Lang Publishing, Incorporated, Peter, 2013.

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Bengesser, Susanne, and Eva Reininghaus. Genetics of Bipolar Disorder. Lang GmbH, Internationaler Verlag der Wissenschaften, Peter, 2013.

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Bengesser, Susanne, and Eva Reininghaus. Genetics of Bipolar Disorder. Lang GmbH, Internationaler Verlag der Wissenschaften, Peter, 2013.

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McEwen, Bruce S., and Natalie L. Rasgon. The Brain and Body on Stress. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190603342.003.0002.

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Neuroscientists have treated the brain in isolation from the rest of the body, while endocrinology and general medicine have viewed the body largely without regard to the influence of systemic physiology and pathophysiology on higher brain centers outside of the hypothalamus and pituitary gland. But now there is greater recognition of brain–body interactions affecting the limbic and cognitive systems of brain and altering systemic physiology; these are conceptualized as allostasis and allostatic load and overload. These concepts look at both the interactions of brain and body to stressors and health-promoting and health-damaging behaviors, and they help integrate behavior and mood with systemic functions. These interactions involve genetic predispositions and epigenetic alterations mediated by circulating steroid and metabolic hormones. Comorbidity and multi-morbidity of disorders will be illustrated by the relationship of systemic and brain insulin resistance to the psychopathology of depression and to the increased risk for dementia.
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Colm, McDonald, ed. The Maudsley family study of psychosis: A quest for intermediate phenotypes. Hove, East Sussex: Psychology Press, 2008.

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McDonald, Colm. Maudsley Family Study of Psychosis: A Quest for Intermediate Phenotypes. Taylor & Francis Group, 2008.

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McDonald, Colm. Maudsley Family Study of Psychosis: A Quest for Intermediate Phenotypes. Taylor & Francis Group, 2008.

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Book chapters on the topic "Predisposition to depression"

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Müller, Walter E., Birgit Bering, and Hans W. Moises. "Relation Between m-Cholinoceptor Density on Human Blood Cells and Psychological Predisposition Factors for Depression." In New Directions in Affective Disorders, 75–78. New York, NY: Springer New York, 1989. http://dx.doi.org/10.1007/978-1-4612-3524-8_16.

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Toy, Ozan, Emmalee Boyle, and Lynn E. DeLisi. "Inflammatory mechanisms, the immune system, and psychiatric illness." In Landmark Papers in Psychiatry, edited by Elizabeth Ryznar, Aderonke B. Pederson, Mark A. Reinecke, and John G. Csernansky, 81–98. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198836506.003.0005.

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The association between the immune system and mental illnesses has been studied extensively over the years. Specifically, inflammation or abnormalities in immune system factors have been linked to stress, depression, and schizophrenia. The incidence of schizophrenia has been observed to be increased following viral epidemics, and the presence of increased antibodies to viral and other infectious agents has been linked to the illness. In this chapter, the landmark studies supporting the association between inflammation and mental illness are cited, from the early epidemiological studies of viral epidemics, to searches in post-mortem brains for gliosis, to genetic predisposition, and, most recently, to direct evidence of inflammation by measurement of free-water content in magnetic resonance imaging (MRI). Ultimately, medications that restore the immune system may lead to improvement of the major psychiatric disorders.
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Conference papers on the topic "Predisposition to depression"

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Hamilton, Odessa S., Andrew Steptoe, and Olesya Ajnakina. "OP54 Polygenic predisposition, sleep duration, and depression: evidence from a prospective population-based cohort*." In Society for Social Medicine Annual Scientific Meeting Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jech-2022-ssmabstracts.53.

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Fedosova, Ekaterina, Alla Shatskova, and Karine Sarkisova. "REVERSAL LEARNING IN A COMPLEX MAZE IN TWO MONTHS OLD WAG/Rij RATS WITH GENETIC PREDISPOSITION TO ABSENCE-EPILEPSY WITH COMORBID DEPRESSION." In XVI International interdisciplinary congress "Neuroscience for Medicine and Psychology". LLC MAKS Press, 2020. http://dx.doi.org/10.29003/m1300.sudak.ns2020-16/476-477.

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Butova, Tatiana, Oleksiy Denysov, Tetiana Sprynsian, and Dmytro Butov. "Predisposition to the development of depressive states in patients with M/XDR TB." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.499.

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"Effect of overexpression of the 5-HT7 receptor gene on behavior and brain serotonin system in ASC mice with predisposition to depressive-like behavior." In Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-234.

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