Abstract
Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are found in familial and idiopathic cases of Parkinson's disease (PD), but are also associated with immune-related disorders, notably Crohn's disease and leprosy. Although the physiological function of LRRK2 protein remains largely elusive, increasing evidence suggests that it plays a role in innate immunity, a process that also has been implicated in neurodegenerative diseases, including PD. Innate immunity involves macrophages and microglia, in which endogenous LRRK2 expression is precisely regulated and expression is strongly up-regulated upon cell activation. This brief report discusses the current understanding of the involvement of LRRK2 in innate immunity particularly in relation to PD, critically examining its role in myeloid cells, particularly macrophages and microglia.
Highlights
Parkinson’s disease (PD) is a complex, multifactorial neurodegenerative disease
Key PD-associated genes, α-synuclein (SNCA), PARK2, deglycase (DJ-1), leucine-rich repeat kinase 2 (LRRK2), and glucocerebrosidase (GBA), are all expressed in immune cells, implying their potential role in immunity
The substantia nigra pars compacta (SNpc) is one of the brain regions with the highest density of microglia and a relatively low density of astrocytes [11,12]. These factors suggest that the feedforward cycle of chronic activation of microglia and chronic damage of dopaminergic neurones would be detrimental in the SNpc
Summary
Parkinson’s disease (PD) is a complex, multifactorial neurodegenerative disease. In North America, it affects 1.5% of the population over the age of 65. Key PD-associated genes, α-synuclein (SNCA), PARK2, deglycase (DJ-1), leucine-rich repeat kinase 2 (LRRK2), and glucocerebrosidase (GBA), are all expressed in immune cells, implying their potential role in immunity
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