Objective: Given that Parkinson’s disease (PD) may be associated with TREM2 and given that a soluble TREM2 (sTREM2) isoform has been described as elevated in the cerebrospinal fluid (CSF) of Alzheimer’s disease (AD), it was hypothesized that we would also observe an elevated CSF sTREM2 in PD. Secondarily, we were interested in the relationship between sTREM2 levels and blood brain barrier (BBB) integrity and other measures of central and peripheral inflammation in both PD and AD.

Background: PD has been genetically and pathologically associated with neuroinflammation. Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial receptor involved in innate immunity. TREM2 rare protein coding genetic variants have been linked to AD. There is also previous evidence that there is a relationship between PD and TREM2.

Methods: Healthy controls, PD and AD patients donated cerebrospinal fluid (CSF) and plasma to the Cleveland Clinic Lou Ruvo Center for Brain Health Biobank. Inflammatory and BBB biomarkers were measured using a Luminex System, Millipore assays and clinical core services.

Results: We confirmed a previous finding of elevated sTREM2 in the CSF of AD, but this was not observed in PD. Consistent with previous findings, CSF A 40 and 42 were significantly lower in PD versus controls, but CSF total tau and p-tau were no different between controls and PD. We did not find a consistent association of peripheral or central markers of inflammation and CSF sTREM2 in any study group, suggesting a limited impact of general inflammation on CSF sTREM2 levels. While there was a significant positive correlation between CRP and plasma sTREM2 levels in PD, we did not observe correlations with other markers of inflammation and CSF or plasma sTREM2 in PD. There was no difference between PD and normal controls for either peripheral or central markers of inflammation.

Conclusions: We confirmed the finding of elevated sTREM2 in AD, but did not see clear evidence of a relationship between sTREM2 and PD. Taken together, these results do not support a strong role of sTREM2 in the pathophysiology of PD. Despite our findings, further and more expansive studies of inflammatory biomarkers in PD are warranted.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/soluble-trem2-and-central-and-peripheral-inflammatory-biomarkers-in-parkinsons-disease/