Cognitive Reserve in Parkinson's Disease without Dementia: β‐Amyloid and Metabolic Assessment

Abstract

AbstractBackgroundCognitive reserve (CR) is the mismatch between preserved cognition and neuropathological damage. Amyloidopathy in Parkinson's disease (PD) could be associated with faster progression to dementia, but the putative protective effect of CR is unknown.ObjectivesTo evaluate the effect of CR on β‐amyloid burden and brain metabolism in non‐demented PD subjects.MethodsParticipants with PD (n = 53) underwent a clinical evaluation, [18F]‐fluorodeoxyglucose and [18F]‐flutemetamol positron emission tomography magnetic resonances, and were classified according to CR. The metabolic pattern of 16 controls was compared to PD subjects.ResultsThe PD subjects showed hypometabolism mainly in the bilateral posterior cortex. Superior‐CR subjects (n = 22) exhibited better cognitive performance, increased amyloid burden, and higher metabolism in several right hemisphere areas compared to low‐medium‐CR subjects (n = 31).ConclusionsHigher CR in non‐demented PD is associated with better cognitive performance, which might reduce vulnerability to the effect of β‐amyloid. Whether superior CR leads to protection against metabolic deterioration, and predominantly right hemisphere involvement, deserves further exploration.