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• W2113757421 abstract "Background: Carriers of the Huntington disease (HD) mutation develop a progressive neurodegenerative disorder after a pre‐clinical phase. We examined the value of 11 C‐raclopride PET (RAC) as a biomarker for pre‐clinical HD pathophysiology. Methods: In a prospective cohort study with clinical and neuropsychological assessment we collected complete RAC data in 18 pre‐clinical mutation carriers (HD‐PMC) and 11 controls. Follow‐up was 2 years. We calculated striatal RAC binding potential (BP) to measure dopamine D2 receptor availability. Results: No HD‐PMC had overt neuropsychological dysfunction. RAC‐BP in putamen was abnormal in up to 44% of HD‐PMC. The rate of RAC‐BP decline (2.6% per year) was not significantly higher than in controls. Follow‐up putaminal BP correlated weakly with predicted distance to onset of clinical HD ( P = 0.034), but the rate of decline did not. Three HD‐PMC developed motor abnormalities suspect for HD but did not show an increased rate of decline of putaminal BP. Conclusions: Many HD‐PMC have striatal abnormalities but we found no clearly increased rate of D2 receptor changes around the onset of clinical HD. A longer follow‐up of the present study cohort is needed to establish the value of RAC‐BP in assessing the risk of clinical conversion from striatal D2 binding data." @default.
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• W2113757421 date "2009-01-14" @default.
• W2113757421 modified "2023-10-10" @default.
• W2113757421 title "Changes in striatal dopamine D2 receptor binding in pre-clinical Huntington’s disease" @default.
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• W2113757421 doi "https://doi.org/10.1111/j.1468-1331.2008.02390.x" @default.
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