Posterior accumulation of tau and concordant hypometabolism in an early-onset Alzheimer's disease patient with presenilin-1 mutation
Författare
Summary, in English
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.
Publiceringsår
2016-03-15
Språk
Engelska
Sidor
339-343
Publikation/Tidskrift/Serie
Journal of Alzheimer's Disease
Volym
51
Issue
2
Dokumenttyp
Artikel i tidskrift
Förlag
IOS Press
Ämne
- Neurology
Nyckelord
- Alzheimer's disease
- positron-emission tomography
- presenilins
- tau proteins
Status
Published
ISBN/ISSN/Övrigt
- ISSN: 1387-2877