Affiliations: [a] Departments of Neurology, Skåne University Hospital, Lund-Malmö, Sweden
| [b] Memory Clinic, Ängelholm Hospital, Ängelholm, Sweden
| [c] Radiation Physics, Skåne University Hospital, Lund-Malmö, Sweden
| [d] Clinical Neurophysiology, Skåne University Hospital, Lund-Malmö, Sweden
| [e] Clinical Physiology and Nuclear Medicine, Skåne University Hospital, Lund-Malmö, Sweden
| [f] Memory and Aging Center, Department of Neurology, University of California, San Francisco, CA, USA
| [g] Memory clinic, Skåne University Hospital, Lund-Malmö, Sweden
Correspondence:
[*]
Correspondence to: Ruben Smith, Department of Neurology, Skåne University Hospital, Getingev. 4, SE-22185, Lund, Sweden. Tel.: +46 46 171852; Mobile: +46702765214; Fax: +4646177940; E-mail: [email protected].
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
