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• W128663618 abstract "OBJECTIVE: To evaluate the expression of PDE10A using a PET imaging ligand (18F-MNI-659) in Huntington9s disease (HD) and healthy volunteers (HV). BACKGROUND: In Huntington9s disease (HD) degeneration of medium spiny neurons and striatal volume loss are prominent pathological findings. PDE10A is highly expressed in the striatal medium spiny neurons. Inhibition of PDE10A has been identified as a potential disease modifying mechanism for HD. Development of MNI-659, a PDE10A PET radiotracer, offers the potential both to investigate PDE10A expression in HD and to evaluate drug occupancy for PDE10A candidate therapeutics. DESIGN/METHODS: Subjects with HD (n=5) and HV (n=5) were characterized clinically with standard HD scales and completed 18F-MNI-659 PET imaging. Subjects received 5 mCi (±0. 5) 18F-MNI-659 and serial dynamic PET projection data was acquired over 1.5 hrs. Binding potentials (BPnd) were measured for caudate, putamen, globus pallidus and striatum based on pharmacokinetic modeling using cerebellum as a reference region. RESULTS: Mean age and gender for HD 63yrs (58-67) 4F:1M, and for HV 36yrs (29-46) 1F:4M. HD subjects had mild-moderate disease with means (range) on the following scales: total UHDRS 29.4 (18-46), UHDRS chorea score 8.8 (6-12), UHDRS behavioral score 7.5 (2-23), total functional capacity 11 (9-13), Independence Scale 92 (80-100) and MMSE 28.4 (27-30). 18F-MNI-659 mean BPnd for HD compared to HV by region: caudate HD 0.73, HV 2.13; putamen HD 1.41, HV 3.74; globus pallidus HD 1.60, HV 3.52; striatum HD 1.10, HV 2.93. CONCLUSIONS: In this pilot study, 18F-MNI-659 PET shows a markedly reduced binding (60-70%) in HD compared to HV with the most pronounced reduction in the caudate, consistent with expected pathological changes in HD. These data suggest a marked reduction in PDE10A expression in mild subjects. Ongoing studies will examine MNI-659 in pre-symptomatic HD to further explore the change in PDE10A expression in HD. Supported by: In part by Pfizer, Inc. Disclosure: Dr. Jennings has received personal compensation for activities with Lundbeck. Dr. Barret has received personal compensation for activities with Molecular NeuroImaging as an employee. Dr. Friedman has received personal compensation for activities with Teva Neuroscience, Boehringer Ingelheim Pharmaceuticals, Inc., Genzyme Corporation, Adix, Roche Diagnostics Corporation. Dr. Friedman has received research support from Teva Neuroscience, Merck & Co., Inc., EMD Serono, Schering-Plough Corporation, National Institutes of Health, Michael J. Fox Foundation, GE Healthcare and Acadia. Dr. Russell has received personal compensation for activities with Molecular NeuroImaging, LLC, Teva Neuroscience, Boehringer Ingelheim Pharmaceuticals, Inc. as a speaker. Dr. Tamagnan has received personal compensation for activities with Molecular Neuroimaging as an employee. Dr. Alagille has nothing to disclose. Dr. Seibyl has received personal compensation for activities with Bayer Healthcare and GE healthcare as consultant. Dr. Seibyl has received compensation for serving on the board of Molecular Neuroimaging. Dr. Marek has received personal compensation for activities with GE healthcare, Eli Lilly, Astra Zeneca, Merck, and Sanofi. Dr. Marek holds stock and/or stock options in Molecualr Neuroimaging." @default.
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• W128663618 date "2013-02-12" @default.
• W128663618 modified "2023-09-27" @default.
• W128663618 title "Evaluation of Phosphodiesterase 10A (PDE10A) Using MNI-659 PET Imaging in Huntington's Disease (P07.212)" @default.
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