Striatal and Cortical [beta]-Amyloidopathy and Cognition in Parkinson's Disease

• Published in: Movement disorders Vol. 31; no. 1; p. 111
• Main Authors: Shah, Neha, Frey, Kirk A, L.T.M Muller, Martijn, Petrou, Myria, Kotagal, Vikas, Koeppe, Robert A, Scott, Peter JH, Albin, Roger L, Bohnen, Nicolaas I
• Format: Journal Article
• Language: English
• Published: Hoboken Wiley Subscription Services, Inc 01.01.2016
• Subjects: Movement disorders
• ISSN: 0885-3185; 1531-8257
• DOI: 10.1002/mds.26369

Introduction Although most previous cognitive studies of [beta]-amyloidopathy in PD focused on cortical plaque deposition, recent postmortem studies point to an important role of striatal [beta]-amyloid plaque deposition. The aim of this study was to investigate the relative contributions of striatal and cortical [beta]-amyloidopathy to cognitive impairment in PD. Methods Patients with PD (n = 62; age, 68.9 ± 6.4 years; H & Y stage: 2.7 ± 0.5; MoCA score: 25.2 ± 3.0) underwent [11C]Pittsburgh compound B [beta]-amyloid, [11C]dihydrotetrabenazine monoaminergic, and [11C]methyl-4-piperidinyl propionate acetylcholinesterase brain PET imaging and neuropsychological assessment. [11C]Pittsburgh compound B [beta]-amyloid data from young to middle-aged healthy subjects were used to define elevated [11C]Pittsburgh compound B binding in patients. Results Elevated cortical and striatal [beta]-amyloid deposition were present in 37% and 16%, respectively, of this predominantly nondemented cohort of patients with PD. Increased striatal [beta]-amyloid deposition occurred in half of all subjects with increased cortical [beta]-amyloid deposition. In contrast, increased striatal [beta]-amyloid deposition did not occur in the absence of increased cortical [beta]-amyloid deposition. Analysis of covariance using global composite cognitive z scores as the outcome parameter showed significant regressor effects for combined striatal and cortical [beta]-amyloidopathy (F = 4.18; P = 0.02) after adjusting for covariate effects of cortical cholinergic activity (F = 5.67; P = 0.02), caudate nucleus monoaminergic binding, duration of disease, and age (total model: F = 3.55; P = 0.0048). Post-hoc analysis showed significantly lower cognitive z score for combined striatal and cortical [beta]-amyloidopathy, compared to cortical-only [beta]-amyloidopathy and non-[beta]-amyloidopathy subgroups. Conclusions The combined presence of striatal and cortical [beta]-amyloidopathy is associated with greater cognitive impairment than cortical [beta]-amyloidopathy alone in PD. © 2015 International Parkinson and Movement Disorder Society