In addition, the fucosterol-induced decrease in the phosphorylation of JNK following sAβ1-42 treatment was reduced by the blockade of TrkB receptors with cyclotraxin B (200 nM) and the inhibition of PI3K and ERK1/2 activation with LY294002 (20 μM) and SL327 (10 μM), respectively, as shown in Figure 3B. Activation of TrkB signaling has been implicated in neuronal survival, synaptic plasticity, and neurodegenerative diseases [31]. This evidence concerns the gene MAPK3 and neurodegenerative disease.