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Interleukin-1β: a new regulator of the kynurenine pathway affecting human hippocampal neurogenesis.

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TLDR
It is shown for the first time how IL-1β, a pro-inflammatory cytokine shown to be increased in depressed patients, decreases neurogenesis in human hippocampal progenitor cells, and inhibition of the kynurenine pathway may provide a new therapy to revert inflammatory-induced reduction in Neurogenesis.
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This article is published in Neuropsychopharmacology.The article was published on 2012-03-01 and is currently open access. It has received 321 citations till now. The article focuses on the topics: Kynurenine pathway & Kynurenine.

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Citations
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Kynurenines in the mammalian brain: when physiology meets pathology

TL;DR: With recently developed pharmacological agents, it is now possible to restore metabolic equilibrium and envisage novel therapeutic interventions on the basis of the kynurenine pathway.
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Childhood Trauma and Adulthood Inflammation: A Meta-Analysis of Peripheral C-reactive Protein, interleukin-6 and Tumour Necrosis factor-α

TL;DR: It is demonstrated that childhood trauma contributes to a pro-inflammatory state in adulthood, with specific inflammatory profiles depending on the specific type of trauma.
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The inflammasome: Pathways linking psychological stress, depression, and systemic illnesses

TL;DR: The evidence suggests that the inflammasome may be a new target for the development of treatments for depression, as well as psychosomatic and somato-psycho diseases.
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The role of pro-inflammatory cytokines in neuroinflammation, neurogenesis and the neuroendocrine system in major depression.

TL;DR: Although current evidence strongly suggests that cytokines and GRs have important roles in depression, they are essential components of a whole system of inflammatory and endocrine interactions, rather than playing independent parts.
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Neuroinflammation and depression: A review

TL;DR: The intricated dynamic crosstalk between neuro inflammation and other relevant neurobiological correlates of depression add to evidence that neuroinflammation may be a key therapeutic target for future therapeutic strategies in major depressive disorder.
References
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Journal ArticleDOI

A new mathematical model for relative quantification in real-time RT-PCR.

TL;DR: This study enters into the particular topics of the relative quantification in real-time RT-PCR of a target gene transcript in comparison to a reference gene transcript and presents a new mathematical model that needs no calibration curve.
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From inflammation to sickness and depression: when the immune system subjugates the brain

TL;DR: In response to a peripheral infection, innate immune cells produce pro-inflammatory cytokines that act on the brain to cause sickness behaviour, which can lead to an exacerbation of sickness and the development of symptoms of depression in vulnerable individuals.
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The Ki‐67 protein: From the known and the unknown

TL;DR: Although the Ki‐67 protein is well characterized on the molecular level and extensively used as a proliferation marker, the functional significance still remains unclear; there are indications, however, that Ki‐ 67 protein expression is an absolute requirement for progression through the cell‐division cycle.
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Biologic basis for interleukin-1 in disease

TL;DR: This is a lengthy review, with 586 citations chosen to illustrate specific areas of interest rather than a compendium of references, which summarizes what the author considers established or controversial topics linking the biology of IL-1 to mechanisms of disease.
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Inflammation and Its Discontents: The Role of Cytokines in the Pathophysiology of Major Depression

TL;DR: Preliminary data from patients with inflammatory disorders, as well as medically healthy depressed patients, suggest that inhibiting proinflammatory cytokines or their signaling pathways may improve depressed mood and increase treatment response to conventional antidepressant medication.
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