A florbetapir (F18) amyloid PET imaging study in Parkinson's disease dementia: the influence of amyloid deposition on cognitive status and course of disease progression

Introduction: The biological basis for dementia in Parkinson's Disease (PD) appears to be multifactorial. Although cortical Lewy bodies are the most robust correlate, the comorbid Alzheimer's Disease (AD) pathology has been also associated with PD-Dementia (PDD). The clinical significance of amyloid deposits (Aß) in PD remains still a topic of active investigation. Objective: To determine whether amyloid deposition, as assessed by PET imaging with the Florbetapir F18, can distinguish PDD patients with respect to demographic and clinical parameters and to assess whether regional patterns of amyloid deposition correlate with specific cognitive features. Methods: 21 subjects with PDD underwent standardized neurologic and neuropsychological examinations and florbetapir F18 imaging with PET. The amyloid load was estimated on qualitative and semi-quantitative reading. Voxel-wise standardized uptake value ratio (SUVr) images were calculated using the whole cerebellum as a reference region. Results: Aß+ patients showed a more rapid cognitive decline (yearly MMSE point loss of 3.15 versus 1.12 in the Aß- group, p=0,003) and a poorer performance in the digit span forward (p=0,045), Rey auditory verbal learning test delayed recall (p=0,017), phonemic verbal test fluency (p=0,057) and immediate Rey-Osterrieth complex figure test (p=0,053). No other significant group differences in demographic and clinical variables were observed. Conclusions: The Aß PET could be able to separate a distinct category of PDD patients, with a faster progression of dementia and a different cognitive profile. The α-synuclein could promote amyloid deposition in selective brain regions, modifying the clinical phenotype of PDD patients