PROK2 and peripheral nerve injury: Indeed, the exposure of primary cortical cultures to Aβ1-42 strongly induced PROK2 overexpression in neurons that was significantly decreased by PC1 treatment (Figure 1), impairing the pro-apoptotic signaling and confirming previous data which demonstrate the PC1 ability to reduce PROK2 expression and storage in mice spinal neurons and astrocytes following peripheral nerve injury (Maftei et al., 2014; Lattanzi et al., 2015).