These results show that the development of inflammation in the brain of 3-months-old MPSIIIB mice was primarily the consequence of microglial cell priming involving TLR4 and MyD88.
Because an increase in the number of social interactions is usually considered a measure of reduced anxiety [28], it is likely that the tendency of the decreased duration of contacts shown by the SCR mice was primarily influenced by their downregulated anxiety.
The clinical and pathological phenotype presented in saposin C−/− mice was primarily related to neuronal dysfunction.
We hypothesise that if the habituation profile in 129P3 mice was primarily based on anxiety-related characteristics, anxiolytic treatment should improve the habituation capacity in these mice.
The differential response between resistant and susceptible mice was primarily associated with immune function and our analysis provides evidence for the importance of interferon signalling, interferon-responsive genes and complement-related genes in CM pathogenesis.
The concentration of cytosolic acetyl-CoA in the livers of KO and WT mice was similar, suggesting that the impact on fat and cholesterol production in the KO mice was primarily due to down regulation of key synthetic enzymes, not to a shortage of the primary building blocks.
