Connecting TNF-α Signaling Pathways to iNOS Expression in a Mouse Model of Alzheimer's Disease: Relevance for the Behavioral and Synaptic Deficits Induced by Amyloid β Protein

Reelin-mediated signaling in neuropsychiatric and neurodegenerative diseases

“…Similar findings have been reported for IL6, recently shown to directly modulate Tau phosphorylation via the cdk5/p35 pathway in hippocampal neurons (Quintanilla et al, 2004). TNFα has also been shown to directly induce the production of Aβ peptides in vitro (Yamamoto et al, 2007) and mediate amyloid-induced toxicity both in vitro and in vivo (Li et al, 2004;Medeiros et al, 2007). Moreover, inhibition of TNF receptor signaling in transgenic AD mice results in decreased Aβ plaque formation .…”

Effects of Centrally Administered Etanercept on Behavior, Microglia, and Astrocytes in Mice Following a Peripheral Immune Challenge

“…This contrasts previous reports where continuous peripheral TNF-a antagonism in RA patients improved cognition (Chen et al, 2010), suggesting that chronic rather than a single dose administration is needed to achieve such effects. However, it should be noted that Tobinick et al (2006) and Tobinick and Gross, (2008) observed a rapid improvement in cognition in a small cohort of patients with Alzheimer's disease (AD) following a single dose of peri-spinal etanercept and was supported by animal research on AD models where antagonism of TNF-a by ICV injection had immediate effects on cognition (Medeiros et al, 2007). Additionally, these findings suggest that centrally administered etanercept is more effective in attenuating cognitive impairment in CNS disease models such as AD, which are associated with more substantial cognitive deficits, than in our peripheral inflammatory model induced with a single dose of LPS.…”

Immunohistochemical localization of selected pro-inflammatory factors in uterine myomas and myometrium in women of various ages

“…IL-1b and TNF-a increase the level of iNOS mRNA by transcriptional activation [23]. These cytokines also increase the expression of COX-2, the activity of which is controlled by NOS, particularly by its inducible form [24].…”