The accumulation of Aβ in the brain has a complex and poorly understood impact on the progression of PD pathology. Increased Aβ burden has been associated specifically with cognitive decline symptoms in PD, especially in PD with dementia patients. However other studies have found no association between high Aβ burden and cognitive impairment in PD and so much controversy remains.  

Our study used data from the Parkinson's Progression Marker Initiative (PPMI) cohort. We included 25 de novo idiopathic PD patients and 30 healthy controls who all underwent [18F]-florbetaben scans to measure the density of Aβ in 20 cortical regions of interest (ROIs). We then followed this cohort post-scan for two years, measuring their Montreal Cognitive Assessment (MoCA) scores. This data was analyzed using IBM SPSS version 27 software with linear regression modelling and hierarchical cluster analysis. 

A stepwise linear regression of the PD group revealed a strong adjusted R² of 0.50 in a model explaining 50% of the variance in their MoCA score 1-year post-scan using three ROIs: the left gyrus rectus, the left anterior cingulate cortex, and the right parietal cortex. We also found a cluster in PD where increased Aβ deposition in these ROIs correlated more strongly with cognitive decline. 

The results suggest Aβ does have a moderate association with cognitive decline in PD at predicting future MoCA scores. The inconsistencies in the literature regarding Aβ and PD cognitive decline may be due to the patchwork impact Aβ burden has on different brain regions. Thus, Aβ burden is necessary, but not sufficient, at explaining the cognitive decline symptoms in PD.