Abstract
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.
Highlights
There is increasing evidence of microglia, mediators of the neuroinflammatory mechanisms, involvement in several neurodegenerative diseases [1,2,3]
We investigated if neuroinflammation is present in lrrk2 mutation carriers and we provided preliminary insights into its relation to Parkinson’s disease (PD) development
The factorial analysis of variance (ANOVA) showed no significant differences in age (F(3, 29) = 1.68, p = 0.1), as well as in the 11C-PBR28 injected dose (F(3, 29) = 0.68, p =0.6 0.295) or the specific activity at the time of injection (F(3, 29) = 0.97, p = 0.4)
Summary
There is increasing evidence of microglia, mediators of the neuroinflammatory mechanisms, involvement in several neurodegenerative diseases [1,2,3]. Imaging studies with 11C-PK11195, a first-generation translocator protein (TSPO) tracer, have shown increased microglia activation in the pons, basal ganglia and frontal and temporal cortices, suggesting an anatomically widespread distribution of microglial activation [14]. The authors found that, in the midbrain and putamen, the [11C]PK11195 binding potential levels were inversely correlated with [11C]CFT (a marker of the dopamine transporter density) binding potential values and positively correlated with the severity of motor symptoms, suggesting that neuroinflammation associated with microglial activation may be part of disease progression.[15]
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