Posterior accumulation of tau and concordant hypometabolism in an early-onset Alzheimer's disease patient with presenilin-1 mutation

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.

• Author: Ruben Smith; Moa Wibom; Tomas Olsson; Douglas Hägerström; Jonas Jögi; Gil D. Rabinovici; Oskar Hansson
• Department/s: MultiPark: Multidisciplinary research focused on Parkinson´s disease
• Publishing year: 2016-03-15
• Language: English
• Pages: 339-343
• Publication/Series: Journal of Alzheimer's Disease
• Volume: 51
• Issue: 2
• Links: http://dx.doi.org/10.3233/JAD-151004
• Document type: Journal article
• Publisher: IOS Press
• Topic: Neurology
• Keywords: Alzheimer's disease; positron-emission tomography; presenilins; tau proteins
• Status: Published
• ISBN/ISSN/Other: ISSN: 1387-2877