Objective: To test for any association between amyloid deposition and future cognition in Parkinson’s disease, in a sample enriched for mild cognitive impairment.

Background: Progressive cognitive decline and dementia is common in Parkinson’s disease, and follows a highly variable time course from normal cognitive ability to dementia. Elucidation of subtle pathological differences in early disease may assist estimation of future outcomes. One such pathological change is amyloid deposition, as measured by PET imaging.

Method: We acquired [18F]-Florbetaben (FBB) amyloid PET and structural MRI for 114 patients with Parkinson’s disease, recruited from the Movement Disorders clinic at the New Zealand Brain Research Institute. Participants were classified at baseline as having normal cognition (PDN, n=23), mild cognitive impairment (PD-MCI, n=76), or dementia (PDD, n=15) using the MDS level II criteria. Cortical FBB uptake was expressed in centiloids and as SUVR, using the Centiloid Project whole cerebellum region as a reference. All participants underwent cognitive screening every 6-months and a full neuropsychological battery every year, for up to 3 years. Change in global cognitive performance and conversion status at follow-up will be assessed against baseline amyloid deposition using a bayesian regression model, accounting for baseline cognitive performance, age and sex.

Results: FBB binding was higher in PDD (CL(sd)=42(44)) compared to PDN (CL=16(19)) and PD-MCI (CL=18(27)), but this difference did not survive adjustment for the older age of the PDD group (PDN=70(6)yrs; PD-MCI=72(6)yrs; PDD=77(6)yrs). There was no evidence at baseline of an association of FBB binding with global cognitive scores. Over a median cognitive follow-up time of 2yrs [0-4yrs], 5 participants converted from PDN to PD-MCI, 23 converted from PD-MCI to PDD, and 9 reverted from PD-MCI to PDN. Interim statistical analyses will determine if any correlation exists between baseline amyloid deposition and follow-up cognitive assessments.

Conclusion: The lack of an association between PET amyloid deposition and cognitive impairment at baseline suggests that amyloid pathology is not the primary driver of cognitive impairment in the early stages of Parkinson’s disease. However, there remains the possibility that early brain amyloid burden may yet have an influence on future outcomes in PD.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/amyloid-load-and-cognitive-decline-in-parkinsons-disease-preliminary-longitudinal-findings/