Fig. 7

Working model of PGRN functions presented in the NAc in FTD-like behavior and depression-like behavior. We show that PGRN deficiency-induced FTD-like behavioral deficits correlates with astrocyte activation, neuroinflammatory cytokines disturbances and neuroplasticity increase observing in the NAc. In the NAc neuroinflammation-triggered depressive-like mouse model, PGRN stimulates astrocytes and microglial activation in the NAc, thus promoting neuroinflammatory reaction and neuroplasticity increase presented in the NAc and subsequent depressive-like behaviors via p38 and NF-κB pathways