Relationships between hypometabolism and both β‐amyloid and tau PET in corticobasal syndrome

INTRODUCTION: Alzheimer's disease (AD) pathology causes corticobasal syndrome (CBS) in 21%-50% of patients. Studies have assessed hypometabolism in CBS according to beta-amyloid (A) positron emission tomography (PET), but the understanding of the association of both AD-tau (T) and A with hypometabolism is incomplete. METHODS: Thirty-three CBS patients and 45 controls underwent fluorodeoxyglucose (FDG), flortaucipir, and Pittsburgh compound-B PET and were classified as A +/- and T +/-. FDG-PET uptake was extracted for 12 regions-of-interest in dominant (most affected) and non-dominant hemispheres and compared across A/T groups. RESULTS: A+T+ patients had greater hypometabolism in temporo-parieto-occipital cortices than A+T- and A-T- groups, with no differences observed between the A+T- and A-T- groups. FDG asymmetry was more accentuated in A+T+ patients. Medial temporal and basal ganglia metabolism were similar across AT groups. DISCUSSION: Amyloid and tau positivity contribute synergistically to hypometabolism and asymmetry in temporo-parieto-occipital cortices in CBS, with AD-like patterns of hypometabolism observed only in A+T+ patients.