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• W1572365863 abstract "OBJECTIVE: To evaluate [ 18 F]MNI-659, a highly selective striatal PDE10A PET imaging tracer, as a biomarker for longitudinal studies in early HD. BACKGROUND: PDE10A is specifically expressed in striatal neurons. Several studies indicate PDE10A expression is a sensitive marker of striatal HD pathology. A cross-sectional study demonstrated reduction in [ 18 F]MNI-659 striatal binding that correlated well with clinical and molecular measures of disease severity. DESIGN/METHODS: Eight HD subjects (mean age, 49.5) underwent clinical assessments, UHDRS rating, and brain MRI. The cohort included 2 subjects with premanifest HD, 2 with stage 1 manifest HD, and 4 with stage 2. All subjects underwent 90 minutes of PET imaging following injection of ~5 mCi [ 18 F]MNI-659. Binding potentials were determined for the basal ganglia nuclei with cerebellum as reference. All underwent follow-up [ 18 F]MNI-659 PET imaging and clinical assessments approximately 1 year later. RESULTS: The mean time to follow-up was 14.7 months. The mean UPDRS motor subscale score increased 3.8 points (S.D. ±7.9) and the mean total functional capacity declined 1.1 points (±2.5). Three stage 2 subjects increased to stage 3. As previously seen, the HD cohort had baseline mean [ 18 F]MNI-659 uptake approximately 50[percnt] lower than normal. The mean annualized rates of reduction in [ 18 F]MNI-659 uptake in caudate, putamen, and globus pallidus were 16.59[percnt] (±0.12), 6.91[percnt] (±0.04), and 5.81[percnt] (±0.07), respectively. Substantially less variability was noted in the imaging rates of change compared to clinical measures. CONCLUSIONS: [ 18 F]MNI-659 appears to be an exceptional striatal imaging biomarker for early HD. Reductions in this PDE10A PET biomarker correlated strongly with clinical and molecular markers of early HD. Furthermore, this study demonstrates that [ 18 F]MNI-659 appears to decline at a predictable rate in striatal nuclei across early HD. [ 18 F]MNI-659 PET may be a valuable additional imaging biomarker in observational or interventional HD trials. Study Supported by: Molecular NeuroImaging, LLC Disclosure: Dr. Russell has received personal compensation for activities with Molecular NeuroImaging, LLC as an employee. Dr. Jennings has received personal compensation for activities with Lundbeck Research USA, Inc. and UBC Pharma. Dr. Barret has received personal compensation for activities with Molecular NeuroImaging as an employee. Dr. Tamagnan has received personal compensation for activities with Molecular NeuroImaging as an employee. Dr. Carroll has received personal compensation for activities with Molecular NeuroImaging as an employee. Dr. Alagille has received personal compensation for activities with Molecular NeuroImaging Inc. as an employee. Dr. Morley has received personal compensation for activities with Molecular NeuroImaging as an employee. Dr. Papin has received personal compensation for activities with Molecular NeuroImaging Inc. as an employee. Dr. Seibyl has received personal compensation for activities with Bayer Healthcare, GE Healthcare, and Piramal Imaging as a consultant. Dr. Marek has received personal compensation for activities with Molecular Neuroimaging, GE Healthcare, Piramal Group, Eli Lilly & Company, Merck & Co., Roche Diagnostics Corporation, Pronetha, Novartis, US WorldMeds, and nLife Therapeutics as a consultan" @default.
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• W1572365863 date "2015-04-06" @default.
• W1572365863 modified "2023-09-26" @default.
• W1572365863 title "Monitoring loss of striatal phosphodiesterase 10A (PDE10A) with [18F]MNI-659 and PET: A biomarker of early Huntington disease (HD) progression. (I11-4A)" @default.
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