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Abstract Details

Initial Long-term Treatment with Rotigotine Maintains Striatal Dopamine Transporter Binding in De Novo Patients with Parkinson Disease
Movement Disorders
P5 - Poster Session 5 (5:30 PM-6:30 PM)
10-021
We examined how initial long-term treatment with rotigotine influences dopamine transporter (DAT) binding in de novo patients with Parkinson disease (PD).
The Parkinson’s Progression Marker Initiative study showed the mean DAT binding decline rate of -11% at the first year in very early PD patients (Simuni et al. Move Disord 2018). Rotigotine, a dopamine agonist, has the binding affinity to D2/D3/D4 and D1/D5 receptors. At 12 weeks after its optimal dose, striatal DAT binding was increased at 15-17% in de novo PD patients (Rossi et al. Clin Neuropharmacol 2017). Long- term effects of rotigotine on DAT binding remain unknown.

Twelve de novo PD patients initially received rotigotine (9-18 mg/day). After 20-24 weeks, levodopa/carbidopa (200-300 mg/day) was added in 2 patients. Ten patients continued rotigotine monotherapy for 52 weeks. None had other anti-PD drugs during this study. [123I]FP-CIT single-photon emission computed tomography was performed at baseline and endpoint (52-weeks rotigotine post-administration). Striatal specific binding ratio (SBR) was calculated semiquantitatively using DAT VIEW automated analysis software (Nihon Medi-Physics, Tokyo, Japan) based on Tossici–Bolt’s method. SBR decline rate was calculated as (baseline SBR – endpoint SBR)/baseline SBR×100 (%).

Clinical profile revealed the mean age (SD) of 71.5 (10.6) years, disease duration < 10 months, and Hoehn and Yale stage of 2. The mean (SD) of MDS-UPDRS III was 15.1 (5.2) at baseline and 6.3 (3.1) at endpoint. The mean (SD) of SBR was 3.2 (0.9) at baseline and 3.1 (0.8) at endpoint. The mean SBR decline rate (SD) was -1.5 (5.8)%. Striatal SBR changes did not differ statistically before and after rotigotine treatment.

Initial long-term treatment with rotigotine maintained striatal DAT binding in early PD patients, in addition to clinical improvement. The data supports a therapeutic potential that this medication delays axonal or neuronal degeneration of the nigrostriatal pathway in early PD patients. 
Authors/Disclosures
Ken Ikeda, MD, PhD (Toho University Omori Medical Center)
PRESENTER
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Osamu Kano, MD, PhD (Department of Neurology, Toho University Faculty of Medicine) Dr. Kano has nothing to disclose.
Kiyokazu Kawabe, MD (Department of Neurology Saiseikai Yokohamashi Tobu Hospital) No disclosure on file
Yasuo Iwasaki, MD No disclosure on file