Kinins and microglial responses in bipolar disorder: a neuroinflammation hypothesis

Kinins and microglial responses in bipolar disorder: a neuroinflammation hypothesis

Author Naaldijk, Yahaira M. Google Scholar
Bittencourt, Maria C. Autor UNIFESP Google Scholar
Sack, Ulrich Google Scholar
Ulrich, Henning Google Scholar
Abstract Bipolar disorder (BD) is a severe psychiatric disorder that affects up to 15% of the worldwide population. Characterized by switches in mood between mania and depression, its etiology is still unknown and efforts have been made to elucidate the mechanisms involved in first episode, development and progression of the disorder. Microglia activation, abnormal activity of GSK-3 beta and reduction in neurotrophic factor expression related to neuroinflammatory processes have been indicated to be part of the disorder's pathophysiology. Lithium, the main mood stabilizer used for the treatment and prevention of relapses, acts as an anti-inflammatory agent. Based on that, here we suggest a neuroinflammatory pathway for would be BD progression, in which microglia activation states modulated via constitutive induction of kinin-B1 receptor and reduction of kinin-B2 receptor expression and activity.
Keywords bipolar disorder
kallikrein-kinin system
xmlui.dri2xhtml.METS-1.0.item-coverage Berlin
Language English
Date 2016
Published in Biological Chemistry. Berlin, v. 397, n. 4, p. 283-296, 2016.
ISSN 1431-6730 (Sherpa/Romeo, impact factor)
Publisher Walter De Gruyter Gmbh
Extent 283-296
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000374975000002

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