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

Smith, Ruben LU ; Wibom, Moa LU ; Olsson, Tomas ; Hägerström, Douglas LU ; Jögi, Jonas LU orcid ; Rabinovici, Gil D. and Hansson, Oskar LU orcid (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
; ; ; ; ; and
organization
publishing date
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
  • pmid:26836192
  • wos:000374240000002
  • scopus:84961782665
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
2024-02-18 23:56:33
@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}},
}