Objective: The aim of the study was to examine the potential of the second-generation tau-PET tracer 18F-PI2620 to detect tau deposition in anti-IgLON5 disease.

Background: Anti-IgLON5 disease is rare autoimmune encephalitis typically leading to sleep disorders, bulbar symptoms and gait instability, and is associated with tau-deposition predominantly in the dorsal brainstem and hypothalamus [1].

Method: Four patients with confirmed anti-IgLON5 disease (phenotypes in keeping with the clinical diagnosis and positive antibody testing in CSF) underwent a dynamic 90-minutes PET scan with ¹⁸F-PI2620. After preprocessing (realignment, normalization, calculation of binding potential maps), we generated z-deviation maps of the binding potential in comparison to a healthy control sample and calculated voxel-wise median images of the z maps.

Results: On an individual level, we found tau depositions in the dorsal rostral medulla, cerebellum, hypothalamus and striatum (> 2 standard deviations in z-maps). Figure 1 [figure1] shows the individual z map of a patient with a disease duration of five years. The median z-map image revealed high tau burden in the dorsal rostral medulla oblongata, cerebellum across the group [figure2]

Conclusion: We found initial evidence for pathological tau-tracer uptake in anti-IgLON5 disease using ¹⁸F-PI2620. Future analyses will focus on the correlation between tau pathology, disease duration and phenotype. Furthermore, we plan to extend the cohort and perform longitudinal measurements to examine the role of tau pathology in anti-IgLON5 disease.

References: [1] Gelpi E, Höftberger R, Graus F, et al. Neuropathological criteria of anti-IgLON5-related tauopathy. Acta Neuropathol 2016; 132: 531–543.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/in-vivo-measurement-of-tau-depositions-in-anti-iglon5-disease-with-18f-pi2620-pet/