Microglial activation in Parkinson’s disease using [18F]-FEPPA

摘要

BackgroundNeuroinflammatory processes including activated microglia have been reported to play an important role in Parkinson’s disease (PD). Increased expression of translocator protein (TSPO) has been observed after brain injury and inflammation in neurodegenerative diseases. Positron emission tomography (PET) radioligand targeting TSPO allows for the quantification of neuroinflammation in vivo. MethodsBased on the genotype of the rs6791 polymorphism in the TSPO gene, we included 25 mixed-affinity binders (MABs) (14 PD patients and 11 age-matched healthy controls (HC)) and 27 high-affinity binders (HABs) (16 PD patients and 11 age-matched HC) to assess regional differences in the second-generation radioligand [18F]-FEPPA between PD patients and HC. FEPPA total distribution volume ( V _T) values in cortical as well as subcortical brain regions were derived from a two-tissue compartment model with arterial plasma as an input function. ResultsOur results revealed a significant main effect of genotype on [18F]-FEPPA V _T in every brain region, but no main effect of disease or disease × genotype interaction in any brain region. The overall percentage difference of the mean FEPPA V _T between HC-MABs and HC-HABs was 32.6% (SD?=?2.09) and for PD-MABs and PD-HABs was 43.1% (SD?=?1.21). ConclusionsFuture investigations are needed to determine the significance of [18F]-FEPPA as a biomarker of neuroinflammation as well as the importance of the rs6971 polymorphism and its clinical consequence in PD.