Variability of diffuse plaques and amyloid angiopathy in Parkinson’s disease with mild cognitive impairment

Abstract

We appreciate Professor Jellinger’s correspondence [2] regarding our study [1] and his findings also showing heterogeneity of Lewy body and Alzheimer pathology in an additional eight cases of PD-MCI (four amnestic, four non-amnestic) [2]. Professor Jellinger questioned our lack of data on diffuse (amyloid) plaques and cerebral amyloid angiopathy (CAA), and so those data are presented. As seen in the Table 1, five cases had 3? diffuse amyloid plaque density in the cortex. Caudate-putamen amyloid plaque density ranged from 0 to 2?. While we did not measure CAA in the meninges, we did in multiple cortical regions (frontal, temporal, parietal, and occipital) using a 0–3 scale that was then totaled (maximum possible score = 12). Four cases (3 amnestic, 1 non-amnestic) had CAA score of 0, then one case each had scores of 1 (amnestic), 3 (non-amnestic), 4 (non-amnestic), and 5 (non-amnestic). All the cases with CAA score C 1 had a diffuse amyloid plaque density of 3?. We therefore agree with Professor Jellinger that further data are needed, with multivariate analysis, to determine if diffuse amyloid plaque load and CAA contribute to cognitive impairment in PD.