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J Alzheimers Dis. 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.

Author information

1
Departments of Neurology, Skåne University Hospital, Lund-Malmö, Sweden.
2
Memory Clinic, Ängelholm Hospital, Ängelholm, Sweden.
3
Radiation Physics, Skåne University Hospital, Lund-Malmö, Sweden.
4
Clinical Neurophysiology, Skåne University Hospital, Lund-Malmö, Sweden.
5
Clinical Physiology and Nuclear Medicine, Skåne University Hospital, Lund-Malmö, Sweden.
6
Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA.
7
Memory clinic, Skåne University Hospital, Lund-Malmö, Sweden.

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

PMID:
26836192
DOI:
10.3233/JAD-151004
[Indexed for MEDLINE]

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