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18F-AV-1451 tau PET imaging correlates strongly with tau neuropathology in MAPT mutation carriers

Smith, Ruben LU ; Puschmann, Andreas LU orcid ; Schöll, Michael LU ; Ohlsson, Tomas ; Van Swieten, John ; Honer, Michael ; Englund, Elisabet LU orcid and Hansson, Oskar LU orcid (2016) In Brain 139(9). p.2372-2379
Abstract

Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo. However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. We performed tau positron emission tomography imaging with 18F-AV-1451 in three patients harbouring a p.R406W mutation in the MAPT gene, encoding tau. This mutation results in 3- and 4-repeat tau aggregates similar to those in Alzheimer's disease, and many of the mutation carriers initially suffer from memory impairment and temporal lobe atrophy. Two patients with short disease duration and isolated memory impairment exhibited 18F-AV-1451 uptake mainly in the... (More)

Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo. However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. We performed tau positron emission tomography imaging with 18F-AV-1451 in three patients harbouring a p.R406W mutation in the MAPT gene, encoding tau. This mutation results in 3- and 4-repeat tau aggregates similar to those in Alzheimer's disease, and many of the mutation carriers initially suffer from memory impairment and temporal lobe atrophy. Two patients with short disease duration and isolated memory impairment exhibited 18F-AV-1451 uptake mainly in the hippocampus and adjacent temporal lobe regions, correlating with glucose hypometabolism in corresponding regions. One patient died after 26 years of disease duration with dementia and behavioural deficits. Pre-mortem, there was 18F-AV-1451 uptake in the temporal and frontal lobes, as well as in the basal ganglia, which strongly correlated with the regional extent and amount of tau pathology in post-mortem brain sections. Amyloid-β (18F-flutemetamol) positron emission tomography scans were negative in all cases, as were stainings of brain sections for amyloid. This provides strong evidence that 18F-AV-1451 positron emission tomography can be used to accurately quantify in vivo the regional distribution of hyperphosphorylated tau protein.

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author
; ; ; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Alzheimer's disease, frontotemporal dementia, MAPT R406W mutation, positron emission tomography, tau
in
Brain
volume
139
issue
9
pages
8 pages
publisher
Oxford University Press
external identifiers
  • pmid:27357347
  • wos:000383719500013
  • scopus:84994896458
ISSN
0006-8950
DOI
10.1093/brain/aww163
language
English
LU publication?
yes
id
66003d0e-0b13-46f3-9fce-23f0af114c6d
date added to LUP
2016-12-01 10:27:33
date last changed
2025-03-24 02:43:19
@article{66003d0e-0b13-46f3-9fce-23f0af114c6d,
  abstract     = {{<p>Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo. However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. We performed tau positron emission tomography imaging with <sup>18</sup>F-AV-1451 in three patients harbouring a p.R406W mutation in the MAPT gene, encoding tau. This mutation results in 3- and 4-repeat tau aggregates similar to those in Alzheimer's disease, and many of the mutation carriers initially suffer from memory impairment and temporal lobe atrophy. Two patients with short disease duration and isolated memory impairment exhibited <sup>18</sup>F-AV-1451 uptake mainly in the hippocampus and adjacent temporal lobe regions, correlating with glucose hypometabolism in corresponding regions. One patient died after 26 years of disease duration with dementia and behavioural deficits. Pre-mortem, there was <sup>18</sup>F-AV-1451 uptake in the temporal and frontal lobes, as well as in the basal ganglia, which strongly correlated with the regional extent and amount of tau pathology in post-mortem brain sections. Amyloid-β (<sup>18</sup>F-flutemetamol) positron emission tomography scans were negative in all cases, as were stainings of brain sections for amyloid. This provides strong evidence that <sup>18</sup>F-AV-1451 positron emission tomography can be used to accurately quantify in vivo the regional distribution of hyperphosphorylated tau protein.</p>}},
  author       = {{Smith, Ruben and Puschmann, Andreas and Schöll, Michael and Ohlsson, Tomas and Van Swieten, John and Honer, Michael and Englund, Elisabet and Hansson, Oskar}},
  issn         = {{0006-8950}},
  keywords     = {{Alzheimer's disease; frontotemporal dementia; MAPT R406W mutation; positron emission tomography; tau}},
  language     = {{eng}},
  month        = {{09}},
  number       = {{9}},
  pages        = {{2372--2379}},
  publisher    = {{Oxford University Press}},
  series       = {{Brain}},
  title        = {{<sup>18</sup>F-AV-1451 tau PET imaging correlates strongly with tau neuropathology in MAPT mutation carriers}},
  url          = {{http://dx.doi.org/10.1093/brain/aww163}},
  doi          = {{10.1093/brain/aww163}},
  volume       = {{139}},
  year         = {{2016}},
}