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Abstract Details

Investigation of the Positron-Emission Tomography [18F]MK-6240 Tau Ligand in Genetic Frontotemporal Dementia
Aging, Dementia, and Behavioral Neurology
S23 - Aging and Dementia: Biomarkers and Clinical Trials (3:54 PM-4:06 PM)
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To investigate the potential for the [18F]MK-6240 PET tracer to bind to tau in frontotemporal dementia (FTD).
Tau is one of several proteins which can cause FTD. While knowing which protein is causing a patient’s disease is crucial, no biomarker currently exists for identifying the pathogenic protein in vivo.
We are enrolling subjects with genetic FTD, who constitute an ideal population for testing because their pathology is already known. Each participant undergoes tau-PET scanning with MK-6240, amyloid-PET imaging with NAV-4694 to rule out confounding AD pathology, high-resolution structural MRI, and a battery of neuropsychological tests. We are scanning patients with MAPT mutations (which cause accumulation of tau leading to FTD; therefore these patients are expected to show tau binding) as well as patients with FTD due to mutations such as C9orf72, GRN, and VCP (which cause accumulation of TDP-43; thus these patients are expected to not show abnormal MK-6240 binding).
We have obtained results from eight patients thus far. We have scanned three symptomatic MAPT patients, whose tau-PET scans all demonstrated binding in expected regions without significant off-target binding. We also analysed two asymptomatic MAPT carriers: one, estimated to be five years from disease onset, showed MK-6240 binding especially in anterior frontal and medial temporal lobes; the other was approximately 30 years from disease onset and did not demonstrate any binding. We additionally scanned three individuals with symptomatic FTD caused by a non-tau mutation (one C9orf72; one GRN; one VCP): their scans did not reveal any MK-6240 binding. All amyloid-PET scans were negative.
Our preliminary findings of MK-6240 binding in three symptomatic MAPT patients and one asymptomatic MAPT carrier within five years of disease onset are promising, particularly when combined with the absence of binding in our participants with non-tau mutations. Further patient recruitment is ongoing to determine clinical applicability.
Authors/Disclosures
Jake P. Levy, MD (Department of Neurology, Memorial University of Newfoundland)
PRESENTER 		No disclosure on file
No disclosure on file
Tharick A. Pascoal, Sr., MD, PhD (University of Pittsburgh) Dr. Pascoal has nothing to disclose.
Elizabeth Finger, MD, FAAN Dr. Finger has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Vigil Neuro. Dr. Finger has received personal compensation in the range of $500-$4,999 for serving on a Scientific Advisory or Data Safety Monitoring board for Denali Therapeutics. The institution of Dr. Finger has received research support from CIHR. The institution of Dr. Finger has received research support from Physician Servcices Incorporated. The institution of Dr. Finger has received research support from Weston Foundation. Dr. Finger has received personal compensation in the range of $500-$4,999 for serving as a Annual Meeting Course Director with 好色先生.
No disclosure on file
Pedro Rosa Neto, MD, PhD (McGIll University) Dr. Rosa Neto has received personal compensation in the range of $500-$4,999 for serving as a Consultant for Novo Nordisk.
No disclosure on file