Fig. 7
From: Pathological α-synuclein recruits LRRK2 expressing pro-inflammatory monocytes to the brain
Model for possible LRRK2 interaction with ɑ-synuclein fibrils in neuroinflammation and neurodegeneration. Neuronal terminal damage, caused in part by the fibrillization and aggregation of ɑ-synuclein, may cause microglia and astrocyte responses that deleteriously affect the blood-brain barrier, the secretion of chemokine gradients, or possibly the release of aggregated ɑ-synuclein. Monocyte extravasation may occur with concomitant sensing of ɑ-synuclein fibrils that elicit LRRK2 expression to facilitate chemotaxis into parenchymal tissues. Pro-inflammatory monocytes may control local production of damaging cytokines and oxidative responses to cause further neuronal damage in a feed-forward progressive pathway