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Dysfunction of neurons in the central nervous system is the primary pathological feature of Parkinson's disease (PD). Despite different triggering, emerging evidence indicates that neuroinflammation revealed through microglia activation is critical for PD. Moreover, recent investigations sought a potential relationship between Lrrk2 genetic mutation and microglia activation. In this paper, neuroinflammation in sporadic PD, Lrrk2-PD and unaffected Lrrk2 mutation carriers were investigated. The principal component analysis (PCA) and the subject's residual profile (SRP) techniques were performed on multiple groups and regions of interest in 22 brain-regions. The 11C-PBR28 binding profiles were compared in four genotypes depending on groups, i.e., HC, sPD, Lrrk2-PD and UC, using the PCA and SPR scores. The genotype effect was found as a principal feature of group-dependent 11C-PBR28 binding, and preliminary evidence of a MAB-Lrrk2 mutation interaction in manifest Parkinson's and subjects at risk was found.
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