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Longitudinal plasma p-tau217 is increased in early stages of Alzheimer's disease

Mattsson-Carlgren, Niklas LU orcid ; Janelidze, Shorena LU ; Palmqvist, Sebastian LU orcid ; Cullen, Nicholas LU ; Svenningsson, Anna L. LU orcid ; Strandberg, Olof LU ; Mengel, David ; Walsh, Dominic M. ; Stomrud, Erik LU orcid and Dage, Jeffrey L. , et al. (2020) In Brain : a journal of neurology 143(11). p.3234-3241
Abstract

Plasma levels of tau phosphorylated at threonine-217 (p-tau217) is a candidate tool to monitor Alzheimer's disease. We studied 150 cognitively unimpaired participants and 100 patients with mild cognitive impairment in the Swedish BioFINDER study. P-tau217 was measured repeatedly for up to 6 years (median three samples per person, median time from first to last sample, 4.3 years). Preclinical (amyloid-β-positive cognitively unimpaired, n = 62) and prodromal (amyloid-β-positive mild cognitive impairment, n = 49) Alzheimer's disease had accelerated p-tau217 compared to amyloid-β-negative cognitively unimpaired (β  =  0.56, P < 0.001, using linear mixed effects models) and amyloid-β-negative mild cognitive impairment patients (β  = ... (More)

Plasma levels of tau phosphorylated at threonine-217 (p-tau217) is a candidate tool to monitor Alzheimer's disease. We studied 150 cognitively unimpaired participants and 100 patients with mild cognitive impairment in the Swedish BioFINDER study. P-tau217 was measured repeatedly for up to 6 years (median three samples per person, median time from first to last sample, 4.3 years). Preclinical (amyloid-β-positive cognitively unimpaired, n = 62) and prodromal (amyloid-β-positive mild cognitive impairment, n = 49) Alzheimer's disease had accelerated p-tau217 compared to amyloid-β-negative cognitively unimpaired (β  =  0.56, P < 0.001, using linear mixed effects models) and amyloid-β-negative mild cognitive impairment patients (β  =  0.67, P < 0.001), respectively. Mild cognitive impairment patients who later converted to Alzheimer's disease dementia (n = 40) had accelerated p-tau217 compared to other mild cognitive impairment patients (β  =  0.79, P < 0.001). P-tau217 did not change in amyloid-β-negative participants, or in patients with mild cognitive impairment who did not convert to Alzheimer's disease dementia. For 80% power, 109 participants per arm were required to observe a slope reduction in amyloid-β-positive cognitively unimpaired (71 participants per arm in amyloid-β-positive mild cognitive impairment). Longitudinal increases in p-tau217 correlated with longitudinal worsening of cognition and brain atrophy. In summary, plasma p-tau217 increases during early Alzheimer's disease and can be used to monitor disease progression.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Alzheimer’s disease, biomarker, p-tau, p-tau217, plasma
in
Brain : a journal of neurology
volume
143
issue
11
pages
8 pages
publisher
Oxford University Press
external identifiers
  • pmid:33068398
  • scopus:85097570932
ISSN
1460-2156
DOI
10.1093/brain/awaa286
language
English
LU publication?
yes
id
c18e7e90-9886-4c53-9667-34ed3c40ad9b
date added to LUP
2020-12-22 07:02:52
date last changed
2024-04-17 22:20:47
@article{c18e7e90-9886-4c53-9667-34ed3c40ad9b,
  abstract     = {{<p>Plasma levels of tau phosphorylated at threonine-217 (p-tau217) is a candidate tool to monitor Alzheimer's disease. We studied 150 cognitively unimpaired participants and 100 patients with mild cognitive impairment in the Swedish BioFINDER study. P-tau217 was measured repeatedly for up to 6 years (median three samples per person, median time from first to last sample, 4.3 years). Preclinical (amyloid-β-positive cognitively unimpaired, n = 62) and prodromal (amyloid-β-positive mild cognitive impairment, n = 49) Alzheimer's disease had accelerated p-tau217 compared to amyloid-β-negative cognitively unimpaired (β  =  0.56, P &lt; 0.001, using linear mixed effects models) and amyloid-β-negative mild cognitive impairment patients (β  =  0.67, P &lt; 0.001), respectively. Mild cognitive impairment patients who later converted to Alzheimer's disease dementia (n = 40) had accelerated p-tau217 compared to other mild cognitive impairment patients (β  =  0.79, P &lt; 0.001). P-tau217 did not change in amyloid-β-negative participants, or in patients with mild cognitive impairment who did not convert to Alzheimer's disease dementia. For 80% power, 109 participants per arm were required to observe a slope reduction in amyloid-β-positive cognitively unimpaired (71 participants per arm in amyloid-β-positive mild cognitive impairment). Longitudinal increases in p-tau217 correlated with longitudinal worsening of cognition and brain atrophy. In summary, plasma p-tau217 increases during early Alzheimer's disease and can be used to monitor disease progression.</p>}},
  author       = {{Mattsson-Carlgren, Niklas and Janelidze, Shorena and Palmqvist, Sebastian and Cullen, Nicholas and Svenningsson, Anna L. and Strandberg, Olof and Mengel, David and Walsh, Dominic M. and Stomrud, Erik and Dage, Jeffrey L. and Hansson, Oskar}},
  issn         = {{1460-2156}},
  keywords     = {{Alzheimer’s disease; biomarker; p-tau; p-tau217; plasma}},
  language     = {{eng}},
  number       = {{11}},
  pages        = {{3234--3241}},
  publisher    = {{Oxford University Press}},
  series       = {{Brain : a journal of neurology}},
  title        = {{Longitudinal plasma p-tau217 is increased in early stages of Alzheimer's disease}},
  url          = {{http://dx.doi.org/10.1093/brain/awaa286}},
  doi          = {{10.1093/brain/awaa286}},
  volume       = {{143}},
  year         = {{2020}},
}