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Case Reports
. 2016;51(2):339-43.
doi: 10.3233/JAD-151004.

Posterior Accumulation of Tau and Concordant Hypometabolism in an Early-Onset Alzheimer's Disease Patient with Presenilin-1 Mutation

Ruben Smith  1 , Moa Wibom  2 , Tomas Olsson  3 , Douglas Hägerström  4 , Jonas Jögi  5 , Gil D Rabinovici  6 , Oskar Hansson  7
Affiliations
Case Reports

Posterior Accumulation of Tau and Concordant Hypometabolism in an Early-Onset Alzheimer's Disease Patient with Presenilin-1 Mutation

Ruben Smith et al. J Alzheimers Dis. 2016.

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). 18F-flutemetamol PET showed a distribution of amyloid-β fibrils similar to sporadic AD. However, the pattern of tau pathology, revealed using 18F-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 18F-fluorodeoxyglucose-metabolism, indicating neuronal hypometabolism in regions affected by tau aggregates.

Keywords: Alzheimer’s disease; positron-emission tomography; presenilins; tau proteins.

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