Microglial signalling cascades in neurodegenerative disease
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Anti-inflammatory treatment with β-asarone improves impairments in social interaction and cognition in MK-801 treated mice
2019, Brain Research BulletinCitation Excerpt :Hence, the hippocampus is very vulnerable to the excessive levels of IL-1 and IL-1β, or other pro-inflammatory factors (Chen et al., 2008; Pugh et al., 2001). Microglia, the brain’s resident immune cells, produce a various number of cytokines (Gebicke-Haerter, 2001; Hanisch, 2002; Pocock and Liddle, 2001). A previous study reported that the activation of microglia could be induced by repeated administration of MK-801 in rodents (Monji et al., 2013).
Extracellular cytochrome c as an intercellular signaling molecule regulating microglial functions
2017, Biochimica et Biophysica Acta - General SubjectsCitation Excerpt :Thus, extracellular CytC may not only be a marker of excess cellular death associated with TBI and neurodegeneration, but it may also contribute to the neurotoxic conditions associated with adverse microglial activation. Even though we do not know the exact cytotoxins induced by the exposure of cells to LPS and CytC, previous studies have shown that microglia can secrete a mixture of diverse toxic molecules, which depends on the nature of the activating stimuli; thus, microglia have been shown to release tumour necrosis factor-α, several different proteolytic enzymes, glutamate, nitric oxide, superoxide and various prostanoids among others [33,50]. Additionally, the synergistic effects of CytC with inflammatory stimuli such as LPS indicate a possible interplay between this protein and inflammatory signals, which is a common association reported for other DAMPs under neuroinflammatory conditions [68].
Methylene Blue promotes cortical neurogenesis and ameliorates behavioral deficit after photothrombotic stroke in rats
2016, NeuroscienceCitation Excerpt :The exact impact of inflammation on neurogenesis, however, is not fully understood (Das and Basu, 2008). A primary component of neuroinflamation is microglial activation, a result of which is the production and secretion of pro-inflammatory cytokines including TNF-α, IL-1β and IL-6 (Gebicke-Haerter, 2001; Pocock and Liddle, 2001; Liu and Hong, 2003). Accumulation of these pro-inflammatory cytokines is deleterious to neurons, contributing to neurodegeneration (Minghetti, 2005; Cagnin et al., 2006) and potentially stifling neurogenesis (Monje et al., 2003; Koo and Duman, 2008; Keohane et al., 2010; Green et al., 2012).
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