Abstract: It is unclear whether the distribution of tau pathology differs between cases with early-onset familial Alzheimer’s disease (AD) and sporadic AD. We present positron emission tomography (PET) data from a young patient with a presenilin-1 mutation (Thr116Asn). 18 F-flutemetamol PET showed a distribution of amyloid-β fibrils similar to sporadic AD. However, the pattern of tau pathology, revealed using 18 F-AV1451 PET, showed higher uptake in posterior cingulate, precuneus, parietal and occipital cortices compared to late-onset sporadic AD. Further, the tau pathology, but not amyloid pathology, exhibited a very clear inverse relationship with 18 F-fluorodeoxyglucose-metabolism, indicating neuronal hypometabolism in regions affected…by tau aggregates.
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Keywords: Alzheimer’s disease, positron-emission tomography, presenilins, tau proteins