The relative role of the various
Idual contribution of each drug. The relative role of the various inflammatory markers is not clear, nor is the reason why some markers correlated with neurocognitive decline and some did not. It may be a result of the relatively lowC1-inh 0.22 Eotaxin0.52 IL-1 0.18 IL-8 0.45 MCP-1 0.67 C3bc 0.77 FGF 0.17 IL-1RA 0.01 IL-9 0.05 PAI 0.63 C4bc 0.79 G-CSF 0.47 IL-2 0.04 IL-10 0.38 PDGF 0.number of participants (type II error) but as will be seen below, other investigators have also demonstrated correlation between cognitive function and some, but not all, of the inflammatory markers measured. An inverse relationship between plasma concentration of IL-2 and the probability of successful cardioversion after the administration of amiodarone has been demonstrated [36]. In our study, changes in IL-2 correlated with the rate of decline in cognitive function. To the best of our knowledge, the association between AF, neurocognitive function and the inflammatory markers, IL-1RA, IL-9, IL-12 and MIP-1, has not previously been studied. In a recent study in rats, Ribeiro demonstrated that induction of PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/11834444 a proinflammatory state by administration of metylmalonic acid resulted in increased levels of interleukin-1(IL-1? and tumor necrosis factor- (TNF-), both in blood and in the cerebral cortex of the animals, as well as a reduction in spatial orientation [37]. We were unable to show any correlation between inflammatory markers and changes in white matter lesions of the brain. Furthermore, there were no statistically significant correlations between changes in inflammatory mediators and changes in amygdala and hippocampus volume. However, our data indicate that in the treatment group there was a trend towards a decrease in white matter lesions, while the placebo group showed an increase. One possibility is that the smaller initial white matter lesion volume attenuated the treatment effect. Another is that statistical power was insufficient due to the relatively small group of participants. Furthermore, the follow-up time may have been too short to detect differences in progress. The reason why the decline in only some 4-(Benzyloxy)-4-oxobutanoic acid domains and cognitive tests correlated with changes in inflammatory parameters is unclear. One possibility is that there areTCC 0.93 IFN 0.19 IL-5 0.11 IL-13 0.10 TNF- 0.15 PPH0.29 MIP-1 0.37 IL-6 0.55 IL-15 0.56 VEGF 0.40 ETP 0.19 MIP-1 0.01 IL-7 0.69 IL-17 0.36 IP-10 0.Table 5 P values for each inflammatory parameter, pooled across all cognitive testsProperdin 0.56 GM-CSF 0.41 IL-4 0.25 IL-12 0.01 RANTES 0.C1-inh, C1-inhibitor; ETP, endogenous thrombin potential; FGF, fibroblast growth factor; G-CSF, granulocyte colony-stimulating factor; GM-CSF, granulocytemacrophage colony-stimulating factor; IFN, interferon-; IL, interleukin; IL-1RA, interleukin-1 receptor antagonist; IL-1, interleukin-1, IP-10 (also known as C-X-C motif chemokine 10or CXCL10), interferon gamma-induced protein 10; MCP-1 (also known as CCL2), monocyte chemotactic protein-1; MIP-1 (also known as CCL3), macrophage inflammatory protein-1; MIP-1 (also known as CCL4), macrophage inflammatory protein-1; PAI, plasminogen activator inhibitor; PDGF, platelet-derived growth factor; PPH, plasmin peak height; RANTES (also known as CCL5), regulated on activation, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/8833965 normal T cell expressed and secreted; TCC, terminal complement complex; TNF-, tumor necrosis factor-; 4-((2-Hydroxyethyl)(methyl)amino)benzaldehyde VEGF, vascular endothelial growth factor.Lappeg d et al. Journal of Neuroinflammation 2013, 10:78 http://www.jneuroinflammati.
