Background: Hypometabolism of the posterior cingulate cortex (PCC) is an important diagnostic feature of late-onset, amnestic Alzheimer's disease (AD) measured with 18F-fluorodeoxyglucose positron emission tomography (FDG-PET). However, it is unclear whether PCC hypometabolism has diagnostic value in young-onset, non-amnestic variants of AD, which exhibit less pathology in the hippocampus and default mode network.
Objective: Evaluate the prevalence and diagnostic value of PCC hypometabolism in non-amnestic variants of AD.
Methods: We retrospectively identified 60 patients with young-onset, atypical dementia who have undergone a detailed clinical evaluation, FDG-PET, and an amyloid biomarker (amyloid-PET or cerebrospinal fluid analysis). We quantitatively analyzed regional hypometabolism in 70 regions of interest (ROI) using the MIMneuro® software.
Results: Based on a cut-off of z-score < -1.5 for significant PCC hypometabolism, the prevalence of PCC hypometabolism in non-amnestic variants of AD was 65% compared to 28% in clinical variants of frontotemporal dementia (FTD). The ROI with the maximal hypometabolism was the dominant middle temporal gyrus in the language variant of AD (mean z score -2.28), middle occipital gyrus in PCA (-3.24), middle temporal gyrus in frontal AD (-2.70), and angular gyrus in corticobasal syndrome due to AD (-2.31). The PCC was not among the 10 most discriminant regions between non-amnestic variants of AD versus clinical variants of FTD.
Conclusion: We conclude that PCC hypometabolism is not a discriminant feature to distinguish non-amnestic variants of AD from clinical variants of FTD-and should be interpreted with caution in patients with young-onset, non-amnestic dementia.
Keywords: Alzheimer’s disease; FDG-PET; non-amnestic variants of AD; posterior cingulate cortex; primary progressive aphasia.