Biomarkers.

Background: Establishing practical and effective diagnostic pathways for people with cognitive impairment is a crucial international research priority. Traditional (late-phase) analysis of an amyloid-beta (Aβ) PET scan (∼90 minutes after radiotracer injection) provides important information about the presence/absence of underlying Alzheimer's pathology, but no information about brain metabolism/perfusion. Recent work suggests that amyloid-beta PET tracer uptake shortly after injection ('early-phase') closely reflects brain metabolism and perfusion.

Early-phase amyloid PET reproduces metabolic signatures of cognitive decline in Parkinson's disease.

Introduction: Recent work suggests that amyloid beta (Aβ) positron emission tomography (PET) tracer uptake shortly after injection ("early phase") reflects brain metabolism and perfusion. We assessed this modality in a predominantly amyloid-negative neurodegenerative condition, Parkinson's disease (PD), and hypothesized that early-phase F-florbetaben (eFBB) uptake would reproduce characteristic hypometabolism and hypoperfusion patterns associated with cognitive decline in PD.

Methods: One hundred fifteen PD patients across the spectrum of cognitive impairment underwent dual-phase Aβ PET, structural and arterial spin labeling (ASL) magnetic resonance imaging (MRI), and neuropsychological assessments.