Posterior accumulation of tau and concordant hypometabolism in an early-onset Alzheimer's disease patient with presenilin-1 mutation
(2016) In Journal of Alzheimer's Disease 51(2). p.339-343- 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... (More)
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.
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- author
- Smith, Ruben LU ; Wibom, Moa LU ; Olsson, Tomas ; Hägerström, Douglas LU ; Jögi, Jonas LU ; Rabinovici, Gil D. and Hansson, Oskar LU
- organization
- publishing date
- 2016-03-15
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Alzheimer's disease, positron-emission tomography, presenilins, tau proteins
- in
- Journal of Alzheimer's Disease
- volume
- 51
- issue
- 2
- pages
- 5 pages
- publisher
- IOS Press
- external identifiers
-
- scopus:84961782665
- pmid:26836192
- wos:000374240000002
- ISSN
- 1387-2877
- DOI
- 10.3233/JAD-151004
- language
- English
- LU publication?
- no
- id
- c76221e4-50cd-4b87-b762-60e63df141e9
- date added to LUP
- 2016-06-30 12:29:50
- date last changed
- 2024-09-06 18:45:16
@article{c76221e4-50cd-4b87-b762-60e63df141e9, abstract = {{<p>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). <sup>18</sup>F-flutemetamol PET showed a distribution of amyloid-β fibrils similar to sporadic AD. However, the pattern of tau pathology, revealed using <sup>18</sup>F-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 <sup>18</sup>F-fluorodeoxyglucose-metabolism, indicating neuronal hypometabolism in regions affected by tau aggregates.</p>}}, author = {{Smith, Ruben and Wibom, Moa and Olsson, Tomas and Hägerström, Douglas and Jögi, Jonas and Rabinovici, Gil D. and Hansson, Oskar}}, issn = {{1387-2877}}, keywords = {{Alzheimer's disease; positron-emission tomography; presenilins; tau proteins}}, language = {{eng}}, month = {{03}}, number = {{2}}, pages = {{339--343}}, publisher = {{IOS Press}}, series = {{Journal of Alzheimer's Disease}}, title = {{Posterior accumulation of tau and concordant hypometabolism in an early-onset Alzheimer's disease patient with presenilin-1 mutation}}, url = {{http://dx.doi.org/10.3233/JAD-151004}}, doi = {{10.3233/JAD-151004}}, volume = {{51}}, year = {{2016}}, }