Proteinopathy and Longitudinal Cognitive Decline in Parkinson Disease
Peter S. Myers, John L. O'Donnell, Joshua J. Jackson, Christina N. Lessov-Schlaggar, Rebecca L. Miller, Erin R. Foster, Carlos Cruchaga, Bruno A. Benitez, Paul T. Kotzbauer, Joel S. Perlmutter, Meghan C. Campbell
Abstract
BACKGROUND AND OBJECTIVES: People with Parkinson disease (PD) commonly experience cognitive decline, which may relate to increased α-synuclein, tau, and β-amyloid accumulation. This study examines whether the different proteins predict longitudinal cognitive decline in PD. METHODS: genotype (ε4+, ε4-), which is a risk factor for β-amyloid accumulation. Participants also had comprehensive, longitudinal clinical assessments of overall cognitive function and dementia status, as well as cognitive testing of attention, language, memory, and visuospatial and executive function. We used hierarchical linear growth models to examine whether the different protein metrics predict cognitive change and multivariate Cox proportional hazard models to predict time to dementia conversion. Akaike information criterion was used to compare models for best fit. RESULTS: ) also predicted time to dementia. Models with β-amyloid PET as a predictor fit the data the best. DISCUSSION: Presence or risk of β-amyloid accumulation consistently predicted cognitive decline and time to dementia in PD. This suggests that β-amyloid has high potential as a prognostic indicator and biomarker for cognitive changes in PD.