Cytokine Polymorphisms in the Pathophysiology of Mood Disorders

CNS Spectrums ◽  
2009 ◽  
Vol 14 (8) ◽  
pp. 419-425 ◽  
Author(s):  
Mario Clerici ◽  
Beatrice Arosio ◽  
Emanuela Mundo ◽  
Elisabetta Cattaneo ◽  
Sara Pozzoli ◽  
...  

ABSTRACTIntroduction: An increasing amount of data suggests that dysregulation of the immune system, including the cytokine network, is associated with the etiology and pathophysiology of mood disorders. Genes encoding cytokines are highly polymorphic and single nucleotide polymorphisms, associated with increased or reduced cytokine production, have been described. The aim of this study was to define the genetic immunologic scenario associated with major depressive disorder (MDD) and bipolar disorder.Methods: Eighty-four Italian outpatients affected by bipolar disorder type I, bipolar disorder type II, or MDD, and 363 healthy controls were enrolled into the study. We analyzed allele and genotype distribution of −308 (G/A) tumor necrosis factor-α (TNF-α), +874 (T/A) interferon-γ (IFN-γ), -174 (G/C) interleukin (IL)-6, and −1082 (G/A) IL-10 promoter polymorphisms by Polymerase Chain Reaction Sequence Specific Primers technique.Results: We observed different genotype and allele distributions of TNF-α, IFN-γ, and IL-10 polymorphisms in the three groups of patients analyzed. In particular, bipolar II patients were characterized by an absence of adenine (A) high producer allele of TNF-α (P<.001) and a lower percentage of TT high producer genotype of IFN-γ (P <.001); bipolar I individuals showed reduced percentage of AA low producer genotype of IL-10 (P<.001). Both bipolar I and bipolar II patients not carrying guanine (G) high producer IL-6 allele showed a lower mean age at onset (P=.048).Conclusion: These data support the existence of a genetic profile related to pro-inflammatory cytokines in patients affected by mood disorders. The differences observed across the three clinical phenotypes suggest the presence of different pathogenetic mechanisms involved in the susceptibility of phenotypically different mood disorders.

2016 ◽  
Vol 19 (sup2) ◽  
pp. S41-S51 ◽  
Author(s):  
Maja Pantović-Stefanović ◽  
Nataša Petronijević ◽  
Bojana Dunjić-Kostić ◽  
Milica Velimirović ◽  
Tatjana Nikolić ◽  
...  

2021 ◽  
pp. 000486742110200
Author(s):  
Gordon Parker

The 2020 College guidelines for mood disorders banish bipolar II disorder – despite its formal status in Diagnostic and Statistical Manual of Mental Disorders and International Classification of Diseases manuals for more than two decades – and argue that there is no need to partition bipolar disorder into separate sub-types. Their single-entity model is seemingly based on opinion rather than any support from referenced scientific studies. The author challenges the Committee’s model of there being only one bipolar disorder and argues that it presents several clinical management risks, particularly of ‘over-treatment’.


2013 ◽  
Vol 19 (4) ◽  
pp. 474-482 ◽  
Author(s):  
Ceren Hıdıroğlu ◽  
Özlem Demirci Esen ◽  
Zeliha Tunca ◽  
Şehnaz Neslihan Gűrz Yalçìn ◽  
Lauren Lombardo ◽  
...  

AbstractRisk-taking behavior and impulsivity are core features of bipolar disorder. Whether they are part of the inherited aspect of the illness is not clear. We aimed to evaluate risk-taking behavior as a potential endophenotype for bipolar disorders, and its relationship with impulsivity and illness features. The Balloon Analogue Risk Task (BART) and Barratt Impulsiveness Scale-11 (BIS-11) were used to assess risk-taking behavior and impulsivity respectively in 30 euthymic bipolar I patients (BD), their 25 asymptomatic first-degree relatives (BD-R), and 30 healthy controls (HC). The primary BART outcome measure was the behavioral adjustment score (number of pumps after trials where the balloon did not pop minus the number of pumps after trials where the balloon popped). BD (p< .001) and BD-R (p= .001) had similar and significantly lower adjustment scores than HC. Only BD scored significantly higher on BIS-11 total (p= .01) and motor (p= .04) subscales than HC. Neither the BART, nor impulsivity scores associated with illness features. A limitation of this study is medicated patients and a heterogeneous BD-R were included. Riskiness may be a candidate endophenotype for bipolar disorder as it appears independently from illness features, presents similarly in BD and BD-R groups and differs from impulsivity. (JINS, 2013,19, 1–9)


2008 ◽  
Vol 69 (8) ◽  
pp. 1267-1275 ◽  
Author(s):  
K. Mikael Holma ◽  
Tarja K. Melartin ◽  
Irina A. K. Holma ◽  
Erkki T. Isometsä

2019 ◽  
Vol 22 ◽  
pp. 101695
Author(s):  
Nefize Yalin ◽  
Aybala Saricicek ◽  
Ceren Hidiroglu ◽  
Andre Zugman ◽  
Nese Direk ◽  
...  

2019 ◽  
Vol 85 (10) ◽  
pp. S259
Author(s):  
Laagishan Yoganathan ◽  
Manpreet Sehmbi ◽  
Luciano Minuzzi ◽  
Benicio N. Frey ◽  
Nicholas A. Bock

2019 ◽  
Vol 29 ◽  
pp. S900
Author(s):  
Euijung Ryu ◽  
Gregory Jenkins ◽  
Jared Evans ◽  
Ana Andreazza ◽  
Marquis Vawter ◽  
...  

2009 ◽  
Vol 50 (1) ◽  
pp. 9-12 ◽  
Author(s):  
Ricardo Alexandre Toniolo ◽  
Sheila C. Caetano ◽  
Patrícia Viana da Silva ◽  
Beny Lafer

2018 ◽  
Vol 46 (3) ◽  
pp. 1241-1251 ◽  
Author(s):  
Tinghong Ye ◽  
Tingting Wang ◽  
Xiaoxue Yang ◽  
Xiaoli Fan ◽  
Maoyao Wen ◽  
...  

Background/Aims: Autoimmune hepatitis (AIH) is a chronic necroinflammatory disease of the liver whose pathogenic mechanisms have not yet been elucidated. Moreover, the current treatment used for the vast majority of AIH patients is largely dependent on immunosuppressant administration and liver transplantation. However, research on the pathogenesis of AIH and effective new treatments for AIH have been hampered by a lack of animal models that accurately reproduce the human condition. Methods: AIH models created by concanavalin A (ConA) injections at different times and doses. The levels of ALT, AST, LDH and inflammatory cytokines were examined at various times after 20 mg/kg ConA was administered by ELISA using commercially available kits. Moreover, liver pathological changes were observed by flow cytometry (FCM) and H&E staining. Results: Our experiments demonstrated that the levels of ALT, AST, LDH and several inflammatory cytokines, including TNF-α, IFN-γ, and IL-6, were higher in the 20 mg/kg 12 h ConA group than in the other groups. Importantly, the numbers of activated CD4+ and CD8+ T lymphocytes in the blood, spleen and liver were calculated. These results showed that ConA (20 mg/kg for 12 h)-induced hepatitis was similar to that in clinical AIH patients. Furthermore, we found that the number of MDSCs in the blood was significantly increased in the ConA (20 mg/kg for 12 h) group compared with controls. Our findings indicated that ConA (20 mg/kg for 12 h)-induced hepatitis could be used as an experimental murine model that mirrors most of the pathogenic properties of human type I AIH. Conclusion: This model [ConA (20 mg/kg for 12 h)] provides a valuable tool for studying AIH immunopathogenesis and rapidly assessing novel therapeutic approaches.


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