Primate Monocytes - CD14, CD16 - Ziegler-Heitbrock

LRRK2 contributes to monocyte dysregulation in Parkinson's disease.

Abstract

Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are the most common cause of familial Parkinson’s disease (PD) [20, 32]. Common polymorphisms in LRRK2 have been shown to modulate the risk for sporadic PD [6, 23, 24] strengthening the idea that inherited and sporadic PD share common underlying pathways. Although LRRK2 has been associated with a variety of cellular functions, including autophagy [1], mitochondrial function/dynamics [30] and microtubule/cytoskeletal dynamics [12], the overall physiological function of LRRK2 and its role in PD are only partially understood. Relatively recent studies also support a role for LRRK2 as regulator of inflammation. Substantial levels of LRRK2 protein and mRNA have been reported in immune cells like peripheral blood mononuclear cells (PBMCs), including B-cells, monocytes/macrophages, and dendritic cells [9, 13, 16, 29].