In vivo Imaging of Microglial Activation in Patients with Clinical Suspected Progressive Supranuclear Palsy: A 18FGE180 PET study

Sauerbeck, J.; Beyer, L.; Rohrer, G.; Sonnenfeld, S.; Nübling, G.; Höglinger, G.; Bartenstein, P.; Levin, J.; Rominger, Axel Oliver; Brendel, M. (2018). In vivo Imaging of Microglial Activation in Patients with Clinical Suspected Progressive Supranuclear Palsy: A 18FGE180 PET study. European journal of nuclear medicine and molecular imaging, 45(S1), S267-S267. Springer-Verlag

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Introduction: Progressive supranuclear palsy (PSP) is a
4R-tauopathy with a severe clinical course. The pathophysiological
processes are not sufficiently understood and a causal
therapy for this life limiting disease is still missing. The neuropathological
hallmark of PSP are accumulated tau protein fibrils
that were claimed to be responsible for following neurodegeneration.
Microglial activation has been shown to occur in PSP as
another hallmark of the disease. Therefore, we aimed to establish
in vivo imaging of microglial activity by 18kDa translocator
protein (TSPO) PET. Methods: Seven patients with probable
PSP according to current diagnosis criteria underwent 18FGE180
TSPO PET. All images were scaled by the global mean
and standardized uptake value ratios (SUVR) were generated
in brain regions typically affected in PSP. Voxel-wise differences
were calculated using seven healthy individuals (HC) serving as
controls. Furthermore, we compared patterns of microglial acactivity
with 18F-THK5351 PET (tau/MAO-B ligand) deriving from
previously imaged patients with PSP, matched for age and disease
severity. Results: Significantly increased 18F-GE180 binding
in PSP versus HC was found in the anterior cingulate gyrus
(+22%, p < 0.001), globus pallidus (+14%, p < 0.005), and nucleus
dentatus (+24%, p = 0.001). Voxel-wise microglial activation
matched known regions of disease affection in PSP except
for the midbrain. Contrary 18F-THK5351-PET showed increased
binding predominantly in the midbrain (+19%, p < 0.001) and
binding was also significantly elevated in brain regions with
increased TSPO activity. Conclusion: TSPO-PET imaging in
PSP patients is feasible and patterns of microglial activation
correlated topologically with most brain regions known to be
affected in PSP. The particularly low microglial activation in the
midbrain compared to highest binding of tau/MAO-B ligands
needs further investigation by specific ligands for tau and astrocytosis.

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