Probing the association between dexamethasone-induced cortisol suppression and serotonin transporter availability among drug-free patients with major depressive disorder—A small-sample SPECT study with [123I]ADAM

2013 ◽  
Vol 38 (11) ◽  
pp. 2805-2809 ◽  
Author(s):  
Hsin Chun Tsai ◽  
Shih-Hsien Lin ◽  
I Hui Lee ◽  
Po See Chen ◽  
Kao Chin Chen ◽  
...  
2008 ◽  
Vol 42 (14) ◽  
pp. 1137-1144 ◽  
Author(s):  
Jeffrey M. Miller ◽  
Maria A. Oquendo ◽  
R. Todd Ogden ◽  
J. John Mann ◽  
Ramin V. Parsey

2013 ◽  
Vol 74 (4) ◽  
pp. 287-295 ◽  
Author(s):  
Jeffrey M. Miller ◽  
Natalie Hesselgrave ◽  
R. Todd Ogden ◽  
Gregory M. Sullivan ◽  
Maria A. Oquendo ◽  
...  

1982 ◽  
Vol 141 (4) ◽  
pp. 372-376 ◽  
Author(s):  
Ilana B. Glass ◽  
Stuart A. Checkley ◽  
Eric Shur ◽  
Sheila Dawling

SummaryEleven drug free patients meeting Research Diagnostic Criteria for Major Depressive Disorder have been treated with desipramine and given a clonidine infusion after 0, 1 and 3 weeks of treatment. The sedative and hypotensive effects of clonidine were significantly inhibited after three weeks of treatment with desipramine: a similar interaction was seen after one week of treatment although this just failed to reach statistical significance. The growth hormone (GH) response to clonidine was initially impaired, but increased significantly after one week of treatment. A significant reduction in the GH response occurred during the second and third weeks of treatment with desipramine. This last finding is interpreted as evidence of adaptive change of α2 adrenoceptors: the other changes can be explained by the known ability of desipramine to block the re-uptake of noradrenaline.


2016 ◽  
Vol 51 (1) ◽  
pp. 23-31 ◽  
Author(s):  
Paolo Cassano ◽  
Eric Bui ◽  
Andrew H Rogers ◽  
Zandra E Walton ◽  
Rachel Ross ◽  
...  

Introduction: There is mixed evidence in the literature on the role of inflammation in major depressive disorder. Contradictory findings are attributed to lack of rigorous characterization of study subjects, to the presence of concomitant medical illnesses, to the small sample sizes, and to the limited number of cytokines tested. Methods: Subjects aged 18–70 years, diagnosed with major depressive disorder and presenting with chronic course of illness, as well as matched controls ( n = 236), were evaluated by trained raters and provided blood for cytokine measurements. Cytokine levels in EDTA plasma were measured with the MILLIPLEX Multi-Analyte Profiling Human Cytokine/Chemokine Assay employing Luminex technology. The Wilcoxon rank-sum test was used to compare cytokine levels between major depressive disorder subjects and healthy volunteers, before (interleukin [IL]-1β, IL-6, and tumor necrosis factor-α) and after Bonferroni correction for multiple comparisons (IL-1α, IL-2, IL-3, IL-4, IL-5, IL-7, IL-8, IL-10, IL-12(p40), IL-12(p70), IL-13, IL-15, IFN-γ-inducible protein 10, Eotaxin, interferon-γ, monotype chemoattractant protein-1, macrophage inflammatory protein-1α, granulocyte-macrophage colony-stimulating factor and vascular endothelial growth factor). Results: There were no significant differences in cytokine levels between major depressive disorder subjects and controls, both prior to and after correction for multiple analyses (significance set at p ⩽ 0.05 and p ⩽ 0.002, respectively). Conclusion: Our well-characterized examination of cytokine plasma levels did not support the association of major depressive disorder with systemic inflammation. The heterogeneity of major depressive disorder, as well as a potential sampling bias selecting for non-inflammatory depression, might have determined our findings discordant with the literature.


2019 ◽  
Vol 85 (10) ◽  
pp. S329
Author(s):  
Jeffrey Miller ◽  
Patrick Hurley ◽  
Francesca Zanderigo ◽  
Harry Rubin-Falcone ◽  
R. Todd Ogden ◽  
...  

2019 ◽  
Vol 57 ◽  
pp. 46-51 ◽  
Author(s):  
Suhaer Zeki Al-Fadhel ◽  
Hussein Kadhem Al-Hakeim ◽  
Arafat Hussein Al-Dujaili ◽  
Michael Maes

AbstractObjective:Activation of the immune-inflammatory response system (IRS) and the compensatory immune-regulatory system (CIRS) and aberrations in endogenous opioids play a role in the pathophysiology of major depressive disorder (MDD). There are no studies which examined the associations between both systems in MDD. The aim of the present study was to examine the relation between β-Endorphin (β-EP), Endomorphin-2, and their mu-opioid receptor (MOR) as well as interleukin (IL)-6 and IL-10, an anti-inflammatory cytokine, in MDD patients.Method:The study included 60 depressed drug-free male patients and 30 matched controls. Serum β-EP, Endomorphin-2, MOR, IL-6 and IL-10 levels were measured using ELISA techniques.Results:The results revealed a significant increase in serum β-EP, MOR, IL-6 and IL-10 in MDD patients versus healthy controls. MOR levels were strongly associated with IL-10 levels. There were no significant correlations between endogenous opioids and IL-6 and IL-10.Conclusion:The results show that MOR levels may function as a possible component of the CIRS whilst there is no evidence that β-EP and EM-2 may modify the IRS. The significant correlation between MOR levels and IL-10 may be explained through central activation of the HPA-axis and increased B-cell numbers expressing MOR as a response to cytokine over-secretion in MDD.


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