Glial Activation And Proinflammatory Cytokine In...

Int J Neuropsychopharmacol. 2014 Oct 31;18(3). pii: pyu022. doi: 10.1093/ijnp/pyu022. Quetiapine attenuates glial activation and proinflammatory cytokines in APP/PS1 transgenic mice via inhibition of nuclear factor-ÃŽ ºB pathway. Zhu S1, Shi R1, Li V1, Wang J1, Zhang R1, Tempier A1, He J1, Kong J1, Wang JF1, Li XM2. Author information Abstract BACKGROUND: In Alzheimers disease, growing evidence has shown that uncontrolled glial activation and neuroinflammation may contribute independently to neurodegeneration. Antiinflammatory strategies might provide benefits for this devastating disease. The aims of the present study are to address the issue of whether glial activation and proinflammatory cytokine increases could be modulated by quetiapine†¦show more content†¦Apart from these classic hallmarks, increasing evidence has demonstrated uncontrolled glial activation and neuroinflammation in AD brain may contribute independently to neural dysfunction and cell death (Akiyama et al., 2000; Wyss-Coray and Mucke, 2002). Robust activation of microglia has been found in and around the area of amyloid plaques in the AD brain, and reactive astrocytes have been shown to form a halo surrounding the amyloid plaques (Itagaki et al., 1989; Ho et al., 2005). Additionally, numerous proinflammatory factors have been reported to be elevated in bo th patients with AD and transgenic animal models of AD (Griffin et al., 1989; Akiyama et al., 2000; Ruan et al., 2009). Whether alleviation of neuroinflammation will offer therapeutic benefit for AD remains unclear. Epidemiological studies show a possible association between suppression of inflammation and reduced risk for AD (in t’ Veld et al., 2001; Vlad et al., 2008). Therefore, drugs targeting neuroinflammation might provide benefits for the prevention and treatment of this devastating disease. In the central nervous system, microglia and astrocytes are the major type of glial cells, and activation of these cells has been involved in all neurodegenerative diseases (Wyss-Coray and Mucke, 2002). Nevertheless, the