Candidate Genes Expression Profile Associated with Antidepressants Response in the GENDEP Study: Differentiating between Baseline ‘Predictors' and Longitudinal ‘Targets'
Annamaria Cattaneo,Massimo Gennarelli,Rudolf Uher,Gerome Breen,Anne Farmer,Katherine J. Aitchison,Katherine J. Aitchison,Ian W. Craig,Christoph Anacker,Patricia A Zunsztain,Peter McGuffin,Carmine M. Pariante +11 more
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TLDR
In this article, the leukocyte mRNA expression levels of genes belonging to glucocorticoid receptor (GR) function (FKBP-4, FKBP-5, and GR), inflammatory cytokines (interleukin (IL)-1a, IL-1b), IL-6 and IL-7), macrophage inhibiting factor (MIF), and tumor necrosis factor (TNF)-a), were tested before and after 8 weeks of treatment with escitalopram or nortriptyline, as part of the Genome-About:
This article is published in Neuropsychopharmacology.The article was published on 2013-02-01 and is currently open access. It has received 342 citations till now. The article focuses on the topics: Proinflammatory cytokine.read more
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The role of inflammation in depression: from evolutionary imperative to modern treatment target
TL;DR: Current understanding of the mechanisms by which the innate and adaptive immune systems interact with neurotransmitters and neurocircuits to influence the risk for depression are detailed.
Journal ArticleDOI
So depression is an inflammatory disease, but where does the inflammation come from?
Michael Berk,Lana J. Williams,Lana J. Williams,Felice N. Jacka,Felice N. Jacka,Adrienne O'Neil,Adrienne O'Neil,Julie A. Pasco,Julie A. Pasco,Steven Moylan,Nicholas B. Allen,Amanda L Stuart,Amie C. Hayley,Michelle L. Byrne,Michael Maes,Michael Maes +15 more
TL;DR: The identification of known sources of inflammation provides support for inflammation as a mediating pathway to both risk and neuroprogression in depression.
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Inflammatory cytokines in depression: Neurobiological mechanisms and therapeutic implications
TL;DR: This review explores the idea that specific gene polymorphisms and neurotransmitter systems can confer protection from or vulnerability to specific symptom dimensions of cytokine-related depression and potential therapeutic strategies that target inflammatory cytokine signaling.
Journal ArticleDOI
Association of brain amyloidosis with pro-inflammatory gut bacterial taxa and peripheral inflammation markers in cognitively impaired elderly
Annamaria Cattaneo,Nadia Cattane,Samantha Galluzzi,Stefania Provasi,Nicola Lopizzo,Cristina Festari,Clarissa Ferrari,Ugo Paolo Guerra,Barbara Paghera,Cristina Muscio,Angelo Bianchetti,Giorgio Dalla Volta,Marinella Turla,Maria Cotelli,Michele Gennuso,Alessandro Prelle,Orazio Zanetti,Giulia Lussignoli,Dario Mirabile,Daniele Bellandi,Simona Gentile,Gloria Belotti,Daniele Villani,Taoufiq Harach,Tristan Bolmont,Alessandro Padovani,Marina Boccardi,Giovanni B. Frisoni +27 more
TL;DR: The data indicate that an increase in the abundance of a pro-inflammatory GMB taxon, Escherichia/Shigella, and a reduction in the abundances of an anti-inflammatoryTaxon, E. rectale, are possibly associated with a peripheral inflammatory state in patients with cognitive impairment and brain amyloidosis.
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Cumulative meta-analysis of interleukins 6 and 1β, tumour necrosis factor α and C-reactive protein in patients with major depressive disorder
Rita Haapakoski,Rita Haapakoski,Rita Haapakoski,Julia Mathieu,Klaus P. Ebmeier,Harri Alenius,Mika Kivimäki +6 more
TL;DR: This meta-analysis confirms a robust link between IL-6, CRP and major depression and the role of TNF-α and IL-1β in major depression remains uncertain.
References
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p11 is up-regulated in the forebrain of stressed rats by glucocorticoid acting via two specific glucocorticoid response elements in the p11 promoter.
Lei Zhang,He Li,Tung Ping Su,Jeffery L. Barker,Dragan Maric,Carol S. Fullerton,Maree J. Webster,Christopher J. Hough,Xiao Xia Li,Robert J. Ursano +9 more
TL;DR: It is demonstrated that inescapable tail shock increased both prefrontal cortical p11 mRNA levels and plasma corticosterone levels in rats and it was shown that p 11 mRNA levels were increased in postmortem prefrontal cortical tissue of patients with PTSD.
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The Neuropeptide VGF Is Reduced in Human Bipolar Postmortem Brain and Contributes to Some of the Behavioral and Molecular Effects of Lithium
Smita Thakker-Varia,Ying Y. Jean,Payal Parikh,Caroline F. Sizer,Jennifer Jernstedt Ayer,Ankit Parikh,Thomas M. Hyde,Steven Buyske,Janet Alder +8 more
TL;DR: It is demonstrated using in situ hybridization that VGF is downregulated in bipolar disorder in the CA region of the hippocampus and Brodmann's area 9 of the prefrontal cortex and is necessary for the induction of mitogen-activated protein kinase and Akt by LiCl, thus lending insight into the molecular mechanisms underlying the actions of VGF.
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Biomarkers predicting treatment outcome in depression: what is clinically significant?
TL;DR: This report provides guidance on assessing clinical significance of biomarkers predictive of outcome in depression treatment and recommends a number needed to assess of three suggests that with this effect size, a biomarker will significantly improve the prediction of outcomes in one out of every three patients assessed.
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The prednisolone suppression test in depression: Dose—response and changes with antidepressant treatment
Mario Francisco Juruena,Anthony J. Cleare,Anthony J. Cleare,Andrew Papadopoulos,Andrew Papadopoulos,Lucia Poon,Lucia Poon,Stafford L. Lightman,Carmine M. Pariante +8 more
TL;DR: The response to prednisolone is similar in depressed patients and controls at different doses of prednisOLone, and does not change with symptomatic improvement, in contrast with findings using other measures of hypothalamic-pituitary-adrenal axis function, such as basal cortisol levels or the response to dexamethasone.
Journal ArticleDOI
Serum brain-derived neurotrophic factor and glucocorticoid receptor levels in lymphocytes as markers of antidepressant response in major depressive patients: A pilot study
TL;DR: It is concluded that levels of BDNF in serum and GR levels in lymphocytes may represent biomarkers that could be used to predict responses to venlafaxine treatment, and levels of phospho-CREB (pCREB) did not affect levels of pCREB.