scholarly journals A Review of the Role of Interleukin-2 in the Pathophysiology of Major Depressive Disorder in Hospitalized Patients

2021 ◽  
Vol 6 (3) ◽  
pp. 85-92
Author(s):  
Seyed Alireza Seyed Ebrahimi ◽  
Elham Karamian ◽  
Zahra Sadat Goli ◽  
Leila Sadat Mirseifi

Background: Hospitalization due to any reason or medical condition is associated with fear, anxiety, and depression. Psychological and physiological factors have a significant impact on hospitalization outcomes. Objectives: Given the functional importance of inflammatory cytokines and studies in previous studies on the relationship between inflammatory cytokines and major depressive disorder, we will focus more on studies on the role of interleukin 2 (IL-2) in the pathophysiology of major depressive disorder in hospitalized patients. Methods: We used PubMed, Scopus, and Elsevier databases to search for articles from 1999 to 2021, emphasizing the studies of the last five years. Results: In general, there was no consistent pattern in the observed relationships between cytokine concentrations or changes and clinical signs of significant depression. IL-2 and IL, two receptors in the body, play an essential role in the treatment and the pathophysiology of depression and major depression. Conclusion: Finally, it can be concluded that hospitalization generally exposes the patient to inflammation. Studies show an increased risk of inflammation following hospitalization of patients, and many studies confirm the association of major depression with inflammatory cytokines and, more concentrated, IL-2.

1999 ◽  
Vol 174 (2) ◽  
pp. 112-120 ◽  
Author(s):  
Hartwin S. Sadowski ◽  
Blanca Ugarte ◽  
Israel Kolvin ◽  
Carole E. Kaplan ◽  
Jacqueline Barnes

BackgroundThere is evidence that exposure to social and family disadvantages in childhood are a risk factor for adult depression.AimsTo explore the effects of multiple adversity in early childhood on adult depression, and the relative effects of the different adversities.MethodThis study utilises data from the Newcastle Thousand Family Study. Information on childhood disadvantages was collected when the participants were 5 years old, and information on mental health was gathered when they were 33 years old. Mental health data were scrutinised blind to the evidence of early disadvantage, and best-estimate diagnoses of major depressive disorder were made according to DSM–III–R criteria.ResultsMultiple family disadvantages in childhood substantially increase the risk of suffering a major depressive disorder in adulthood. Such disadvantages include family or marital relationship instability, a combination of poor mothering and poor physical care, and a combination of dependence on social welfare and overcrowding. For females major depression was linked in particular to the quality of parenting in early life.ConclusionsSocial and family (especially multiple family) disadvantages during childhood predispose individuals to an increased risk of major depression in adulthood.


2021 ◽  
Vol 22 ◽  
Author(s):  
Zeyi Huang ◽  
Sijie Tan

Major depressive disorder (MDD) is a common mental disorder. Although the genetic, biochemical, and psychological factors have been related to the development of MDD, it is generally believed that a series of pathological changes in the brain caused by chronic stress is the main cause of MDD. However, the specific mechanisms underlying chronic stress-induced MDD are largely undermined. Recent investigations have found that increased pro-inflammatory cytokines and changes in the inflammatory pathway in the microglia cells in the brain are the potential pathophysiological mechanism of MDD. P2X7 receptor (P2X7R) and its mediated signaling pathway play a key role in microglia activation. The present review aimed to present and discuss the accumulating data on the role of P2X7R in MDD. Firstly, we summarized the research progress in the correlation between P2X7R and MDD. Subsequently, we presented the P2X7R mediated microglia activation in MDD and the role of P2X7R in increased blood-brain barrier (BBB) permeability caused by chronic stress. Lastly, we also discussed the potential mechanism underlying P2X7R expression changes after chronic stress. In conclusion, P2X7R is a key molecule regulating the activation of microglia. Chronic stress activates microglia in the hippocampus by secreting interleukin-1β (IL-1β) and other inflammatory cytokines, and increasing the BBB permeability, thus promoting the occurrence and development of MDD, which indicated that P2X7R might be promising therapeutic target for MDD.


2017 ◽  
Vol 51 (7) ◽  
pp. 711-718 ◽  
Author(s):  
Caroline J Bell ◽  
Joseph M Boden ◽  
L John Horwood ◽  
Roger T Mulder

Objective: Few studies have examined the contribution of specific disaster-related experiences to symptoms of depression. The aims of this study were to do this by examining the roles of peri-traumatic stress and distress due to lingering disaster-related disruption in explaining linkages between disaster exposure and major depressive disorder symptoms among a cohort exposed to the 2010–2011 Canterbury (New Zealand) earthquakes. Methods: Structural equation models were fitted to data obtained from the Christchurch Health and Development Study at age 35 ( n = 495), 20–24 months following the onset of the disaster. Measures included earthquake exposure, peri-traumatic stress, disruption distress and symptoms of major depressive disorder. Results: The associations between earthquake exposure and major depression were explained largely by the experience of peri-traumatic stress during the earthquakes (β = 0.180, p < 0.01) and not by disruption distress following the earthquakes (β = 0.048, p = 0.47). Conclusion: The results suggest that peri-traumatic stress has been under-recognised as a predictor of major depressive disorder.


2008 ◽  
Vol 21 (4) ◽  
pp. 278-286 ◽  
Author(s):  
Tracy S. Hunter

Optimal levels of the bioactive folate are necessary for maintaining proper brain and body functioning. Folate deprivation and impaired folate metabolism are clinically associated with defects in the developing nervous system. Numerous studies implicate a deficiency of bioactive folate with an increased risk of major depressive disorder and other neuropsychiatric disorders. Bioactive forms of folate, particularly L-methylfolate, have been found to augment the therapeutic efficacy of antidepressants in patients with major depressive disorder, who fail to adequately respond to standard therapies. The antidepressant action of L-methylfolate appears to improve treatment outcomes most effectively when administered as an adjuvant to traditional antidepressants. This new understanding of the role of folates in major depressive disorder and other mood disorders offers opportunities to improve treatment outcomes.


Author(s):  
Priya Vishal Naik ◽  
Prachi Datta Dalvi U.

The WHO theme for the year 2017 is Depression. Depression (major depressive disorder) is a common and serious medical illness that negatively affects how a person feels, thinks and behaves. Psychotherapy if incorporated along with medications can be of substantial help in depression. It is also called ‘talking therapy’ and is based on personal interaction with the patient. Patients suffering from this disorder do not easily accept it and hence do not feel the need to seek medical intervention or counselling. In this process the symptoms might get aggravated and suicidal tendency (which is the worst effect of this disease) may develop. So it is extremely essential for the patient, family and society to accept, talk, discuss and seek treatment for this disease. This ‘talking therapy’ is of utmost importance in today’s life where concept of privacy is taking its toll. This therapy is mentioned in Ayurveda as Aashwasan Chikitsa. Aashwasan Chikitsa consists of good, pleasing and benevolent thoughts, spiritual ideas, positive attitude, ethics and communication with near ones. So in the treatment of psychological disorders, along with medications counselling therapy plays a very important role. Finally counselling can act as a part of preventive, curative therapy and also aids to avoid recurrence in the patients of depression.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rona J. Strawbridge ◽  
Keira J. A. Johnston ◽  
Mark E. S. Bailey ◽  
Damiano Baldassarre ◽  
Breda Cullen ◽  
...  

AbstractUnderstanding why individuals with severe mental illness (Schizophrenia, Bipolar Disorder and Major Depressive Disorder) have increased risk of cardiometabolic disease (including obesity, type 2 diabetes and cardiovascular disease), and identifying those at highest risk of cardiometabolic disease are important priority areas for researchers. For individuals with European ancestry we explored whether genetic variation could identify sub-groups with different metabolic profiles. Loci associated with schizophrenia, bipolar disorder and major depressive disorder from previous genome-wide association studies and loci that were also implicated in cardiometabolic processes and diseases were selected. In the IMPROVE study (a high cardiovascular risk sample) and UK Biobank (general population sample) multidimensional scaling was applied to genetic variants implicated in both psychiatric and cardiometabolic disorders. Visual inspection of the resulting plots used to identify distinct clusters. Differences between these clusters were assessed using chi-squared and Kruskall-Wallis tests. In IMPROVE, genetic loci associated with both schizophrenia and cardiometabolic disease (but not bipolar disorder or major depressive disorder) identified three groups of individuals with distinct metabolic profiles. This grouping was replicated within UK Biobank, with somewhat less distinction between metabolic profiles. This work focused on individuals of European ancestry and is unlikely to apply to more genetically diverse populations. Overall, this study provides proof of concept that common biology underlying mental and physical illness may help to stratify subsets of individuals with different cardiometabolic profiles.


2021 ◽  
Vol 11 (1) ◽  
pp. 8
Author(s):  
Carol S. North ◽  
David Baron

Agreement has not been achieved across symptom factor studies of major depressive disorder, and no studies have identified characteristic postdisaster depressive symptom structures. This study examined the symptom structure of major depression across two databases of 1181 survivors of 11 disasters studied using consistent research methods and full diagnostic assessment, addressing limitations of prior self-report symptom-scale studies. The sample included 808 directly-exposed survivors of 10 disasters assessed 1–6 months post disaster and 373 employees of 8 organizations affected by the September 11, 2001 terrorist attacks assessed nearly 3 years after the attacks. Consistent symptom patterns identifying postdisaster major depression were not found across the 2 databases, and database factor analyses suggested a cohesive grouping of depression symptoms. In conclusion, this study did not find symptom clusters identifying postdisaster major depression to guide the construction and validation of screeners for this disorder. A full diagnostic assessment for identification of postdisaster major depressive disorder remains necessary.


2020 ◽  
Author(s):  
Samuel David Clark

AbstractThe kappa opioid receptor (KOR) and its endogenous ligands dynorphins (DYN) have been implicated in the development or symptomatology of a variety of neuropsychiatric disorders. This review covers a brief history of the development of KOR agonists and antagonists, their effects in healthy volunteers, and the potential role of DYN/KOR dysfunction in schizophrenia and major depressive disorder from a translational perspective. The potential role of DYN/KOR dysfunction in schizophrenia is based on several lines of evidence. Selective KOR agonists induce affective states in healthy volunteers with similarities to the symptoms of schizophrenia. Studies have shown increased DYN in patients with schizophrenia, although the data have been mixed. Finally, meta-analytic data have shown that opioid antagonists are associated with reductions in the symptoms of schizophrenia. The potential role of DYN/KOR dysfunction in major depressive disorder is also based on a combination of preclinical and clinical data. Selective KOR agonists have shown pro-depressive effects in human volunteers, while selective KOR antagonists have shown robust efficacy in several preclinical models of antidepressant activity. Small studies have shown that nonselective KOR antagonists may have efficacy in treatment-resistant depression. Additionally, recent clinical data have shown that the KOR may be an effective target for treating anhedonia, a finding relevant to both schizophrenia and depression. Finally, recommendations are provided for translating preclinical models for schizophrenia and major depressive disorder into the clinic.


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