Vikas Kotagal1,2, Nicolaas I Bohnen1,2,3,4, Martijn L T M Müller3,4, Kirk A Frey1,4, Roger L Albin1,2,3. 1. Department of Neurology, University of Michigan, Ann Arbor, MI, USA. 2. Neurology Service and GRECC, VAAAHS, Ann Arbor, MI, USA. 3. University of Michigan Morris K. Udall Center of Excellence for Parkinson's Disease Research, Ann Arbor, MI, USA. 4. Department of Radiology, University of Michigan, Ann Arbor, MI, USA.
Abstract
BACKGROUND: Progression to Hoehn and Yahr (HY) stage 3 marks the transition to advanced disease staging and disability in Parkinson disease (PD). OBJECTIVE/ METHODS: We conducted a case-control study of 36 PD subjects at HY stage 2.5 or 3, with groups matched for gender, age, and disease duration. Positron Emission tomography (PET) imaging included dihydrotetrabenazine [11C]DTBZ and Pittsburgh Compound B [11C]PiB. RESULTS: Subjects with HY 2.5 differed from HY 3.0 in mean cortical PiB distribution volume ratio (1.14 vs. 1.23; Wilcoxon two-sample Z = 2.36, p = 0.024) but not striatal DTBZ PET. CONCLUSION: Cortical amyloid burden differentiates subjects below and at HY stage 3. These results suggest that cortical amyloid accumulation influences the transition from HY2.5 to HY3 and that cortical amyloidopathy may be a therapeutic target in PD.
BACKGROUND: Progression to Hoehn and Yahr (HY) stage 3 marks the transition to advanced disease staging and disability in Parkinson disease (PD). OBJECTIVE/ METHODS: We conducted a case-control study of 36 PD subjects at HY stage 2.5 or 3, with groups matched for gender, age, and disease duration. Positron Emission tomography (PET) imaging included dihydrotetrabenazine [11C]DTBZ and Pittsburgh Compound B [11C]PiB. RESULTS: Subjects with HY 2.5 differed from HY 3.0 in mean cortical PiB distribution volume ratio (1.14 vs. 1.23; Wilcoxon two-sample Z = 2.36, p = 0.024) but not striatal DTBZ PET. CONCLUSION: Cortical amyloid burden differentiates subjects below and at HY stage 3. These results suggest that cortical amyloid accumulation influences the transition from HY2.5 to HY3 and that cortical amyloidopathy may be a therapeutic target in PD.
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