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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 LU ; Hägerström, Douglas LU ; Jögi, Jonas LU ; Rabinovici, Gil D. and Hansson, Oskar LU (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
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
  • 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
2016-11-27 04:41:29
@misc{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},
  keyword      = {Alzheimer's disease,positron-emission tomography,presenilins,tau proteins},
  language     = {eng},
  month        = {03},
  number       = {2},
  pages        = {339--343},
  publisher    = {ARRAY(0x9e98468)},
  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},
  volume       = {51},
  year         = {2016},
}