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

Alzheimer's disease (AD) pathology causes corticobasal syndrome (CBS) in 21%-50% of patients. Studies have assessed hypometabolism in CBS according to β-amyloid (A) positron emission tomography (PET), but the understanding of the association of both AD-tau (T) and A with hypometabolism is incomplete.

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.

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.

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.

Amyloid (A) and tau PET (T) status can be used to stratify CBS patients. A+T+ CBS patients show more hypometabolism in temporo-parieto-occipital cortices. Medial temporal metabolism (typical AD pattern) is similar across AT groups. Parieto-occipital cortices should be assessed when investigating AT pathology in CBS. Amyloid and tau positivity contribute synergistically to hypometabolism and asymmetry in CBS.