%0 Journal Article %J J Alzheimers Dis %D 2016 %T Posterior Accumulation of Tau and Concordant Hypometabolism in an Early-Onset Alzheimer's Disease Patient with Presenilin-1 Mutation. %A Smith, Ruben %A Wibom, Moa %A Olsson, Tomas %A Hägerström, Douglas %A Jögi, Jonas %A Rabinovici, Gil D %A Hansson, Oskar %K Adult %K Age of Onset %K Alzheimer Disease %K Amyloid beta-Peptides %K Aniline Compounds %K Benzothiazoles %K Brain %K Brain Mapping %K Fluorodeoxyglucose F18 %K Humans %K Magnetic Resonance Imaging %K Male %K Positron-Emission Tomography %K Presenilin-1 %K Radiopharmaceuticals %K tau Proteins %X

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.

%B J Alzheimers Dis %V 51 %P 339-43 %8 2016 %G eng %N 2 %1 http://www.ncbi.nlm.nih.gov/pubmed/26836192?dopt=Abstract %R 10.3233/JAD-151004