期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 51, 期 2, 页码 339-343出版社
IOS PRESS
DOI: 10.3233/JAD-151004
关键词
Alzheimer's disease; positron-emission tomography; presenilins; tau proteins
资金
- Swedish Research Council
- European Research Council
- Swedish Brain Foundation
- Swedish Federal Government
- Bundy Academy
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). F-18-flutemetamol PET showed a distribution of amyloid-beta fibrils similar to sporadic AD. However, the pattern of tau pathology, revealed using F-18-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 F-18-fluorodeoxyglucose-metabolism, indicating neuronal hypometabolism in regions affected by tau aggregates.
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