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- W1969488423 abstract "Pro-inflammatory cytokines have been detected in brains of individuals with Alzheimer's disease (AD) and may play a significant role in the pathogenesis of AD. Our earlier reports investigated glial cell responses to LPS and A b, by upregulating the expression of cytokines TNF- a, IL-1 b, and IL-6, as well as iNOS and COX-2. The present study was undertaken to investigate the therapeutic benefits of AICAR (a potent activator of AMP-activated protein kinase) in blocking the pro-oxidant/proinflammatory responses in microglia. Objectives: Our main objectives were a) to understand the activation as well release of cytokines from activated microglia in response to accumulated A b, and possible therapeutic benefits of AICAR. BV-2 microglia were used in these studies to understand LPS/ SMase/A b stimulated signaling mechanisms of NF k B pathway leading to the release of NO, ROS generation , release of inflammatory cytokine (TNF- a, IL-1 b, IL-6) as well the scavenging macrophage like phagocytic functions of microglia. AICAR inhibits LPS, and Smase activated cytokine release and NO production. AICAR also does promote A b phagocytosis. Further we observed a reduction in the stress signaling with a significant lowering in p-ERK, p-p38, p-Akt (ser 473) as well as significant reduction of proteins such as p-NIK, p-IKK a/b and in p-p65 translocation. Microglia play an active role in triggering the immune cytokine responses in the neuro-inflammatory process of AD. AICAR treatment effectively blocked cytokine release, A b phagocytosis by regulating NF k B pathways and perhaps is effective for therapeutics of AD." @default.
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- W1969488423 date "2012-07-01" @default.
- W1969488423 modified "2023-10-16" @default.
- W1969488423 title "P2-376: Therapeutic treatment of AICAR for microglial inflammation in Alzheimer's disease" @default.
- W1969488423 doi "https://doi.org/10.1016/j.jalz.2012.05.1086" @default.
- W1969488423 hasPublicationYear "2012" @default.
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