Alexander F. Santillo (Sweden)
Lund University
Department of Clinical Sciences, Clinical Memory Research Unit
Dr Santillo works as a consultant psychiatrist and is an associate professor at the Clinical Memory Research Unit, Lund University. His research focus is frontotemporal dementia and schizophrenia. His main interest are disease mechanisms and biomarkers, both imaging and fluid biomarkers.

Presenter of 1 Presentation

 Conference Calendar

TAU IMAGING WITH [18F]RO948 PET IN FRONTOTEMPORAL DEMENTIA

Session Name
4330 - SYMPOSIUM: PET 01 (ID 117)
Session Type
SYMPOSIUM
Date
Sat, 01.04.2023
Session Time
08:40 - 10:40
Room
ONSITE - HALL G3
Presenter
Lecture Time
08:55 - 09:10

Abstract

Aims

Frontotemporal dementia (FTD) is in the majority of cases neuropathologically characterized by accumulation of either tau or TDP-43. PET tracers targeted at the protein tau could thus potentially predict underlying protein pathology. We examined the PET tracer [18F]RO948 retention in FTD, aiming to include cases with predictable underlying protein pathology.

Methods

We included 35 patients with FTD: 21 behavioural variant FTD (bvFTD) cases, 11 symptomatic C9orf72 mutations carriers, one patient with non-genetic bvFTD-amyotrophic lateral sclerosis (ALS), one individual with bvFTD due to a GRN mutation and one individual due to a MAPT mutation (R406W). All underwent [18F]RO948 PET and MRI. Two patients also underwent postmortem neuropathological examination. PET tracer retention was examined using a region-of-interest (ROI) and voxel-wise approaches. Comparison subjects were cases of Alzheimer´s disease (AD, n =13) and Aβ-negative cognitively unimpaired individuals (n =13). Tracer binding was also assessed using [3H]RO948autoradiography in six cases not from the present cohort.

Results

[18F]RO948 retention across ROIs was comparable to that in Aβ-negative cognitively unimpaired individuals and clearly lower than in AD. Only minor loci of tracer retention were seen in FTD. Autoradiography did not show any [3H]RO948 binding. AD-like retention levels and specific in-vitro binding was however seen in the R406W MAPT mutation carriers.

Conclusions

[18F]RO948 uptake is not significantly increased in FTD patients and thus cannot predict underlying protein pathology in the majority of cases, with the clear exception being R406W MAPT mutation carriers. [18F]RO948 has however a promising specificity in differentiating AD from FTD.

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