Four distinct trajectories of tau deposition identified in Alzheimer’s disease
(2021) In Nature Medicine 27(5). p.871-881- Abstract
- Alzheimer’s disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. This spreading pattern was thought to be fairly consistent across individuals, although recent work has demonstrated substantial variability in the population with AD. Using tau-positron emission tomography scans from 1,612 individuals, we identified 4 distinct spatiotemporal trajectories of tau pathology, ranging in prevalence from 18 to 33%. We replicated previously described limbic-predominant and medial temporal lobe-sparing patterns, while also discovering posterior and lateral temporal patterns resembling atypical clinical variants of AD. These ‘subtypes’ were stable during longitudinal follow-up and were replicated in a separate... (More)
- Alzheimer’s disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. This spreading pattern was thought to be fairly consistent across individuals, although recent work has demonstrated substantial variability in the population with AD. Using tau-positron emission tomography scans from 1,612 individuals, we identified 4 distinct spatiotemporal trajectories of tau pathology, ranging in prevalence from 18 to 33%. We replicated previously described limbic-predominant and medial temporal lobe-sparing patterns, while also discovering posterior and lateral temporal patterns resembling atypical clinical variants of AD. These ‘subtypes’ were stable during longitudinal follow-up and were replicated in a separate sample using a different radiotracer. The subtypes presented with distinct demographic and cognitive profiles and differing longitudinal outcomes. Additionally, network diffusion models implied that pathology originates and spreads through distinct corticolimbic networks in the different subtypes. Together, our results suggest that variation in tau pathology is common and systematic, perhaps warranting a re-examination of the notion of ‘typical AD’ and a revisiting of tau pathological staging. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/a3e8b18c-1343-4744-b3ff-ca3b1347aeb6
- author
- Vogel, Jacob W.
LU
; Young, Alexandra L.
; Oxtoby, Neil P.
; Smith, Ruben
LU
; Ossenkoppele, Rik
LU
; Strandberg, Olof T.
LU
; La Joie, Renaud
; Aksman, Leon M.
; Grothe, Michel J.
; Iturria-Medina, Yasser
; Pontecorvo, Michael J.
; Devous, Michael D.
; Rabinovici, Gil D.
; Alexander, Daniel C.
; Lyoo, Chul Hyoung
; Evans, Alan C.
and Hansson, Oskar
LU
(Less) - author collaboration
- organization
- publishing date
- 2021
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Nature Medicine
- volume
- 27
- issue
- 5
- pages
- 871 - 881
- publisher
- Nature Publishing Group
- external identifiers
-
- scopus:85105170201
- pmid:33927414
- ISSN
- 1078-8956
- DOI
- 10.1038/s41591-021-01309-6
- language
- English
- LU publication?
- yes
- id
- a3e8b18c-1343-4744-b3ff-ca3b1347aeb6
- date added to LUP
- 2021-09-13 11:25:29
- date last changed
- 2022-05-12 22:03:57
@article{a3e8b18c-1343-4744-b3ff-ca3b1347aeb6,
abstract = {{Alzheimer’s disease (AD) is characterized by the spread of tau pathology throughout the cerebral cortex. This spreading pattern was thought to be fairly consistent across individuals, although recent work has demonstrated substantial variability in the population with AD. Using tau-positron emission tomography scans from 1,612 individuals, we identified 4 distinct spatiotemporal trajectories of tau pathology, ranging in prevalence from 18 to 33%. We replicated previously described limbic-predominant and medial temporal lobe-sparing patterns, while also discovering posterior and lateral temporal patterns resembling atypical clinical variants of AD. These ‘subtypes’ were stable during longitudinal follow-up and were replicated in a separate sample using a different radiotracer. The subtypes presented with distinct demographic and cognitive profiles and differing longitudinal outcomes. Additionally, network diffusion models implied that pathology originates and spreads through distinct corticolimbic networks in the different subtypes. Together, our results suggest that variation in tau pathology is common and systematic, perhaps warranting a re-examination of the notion of ‘typical AD’ and a revisiting of tau pathological staging.}},
author = {{Vogel, Jacob W. and Young, Alexandra L. and Oxtoby, Neil P. and Smith, Ruben and Ossenkoppele, Rik and Strandberg, Olof T. and La Joie, Renaud and Aksman, Leon M. and Grothe, Michel J. and Iturria-Medina, Yasser and Pontecorvo, Michael J. and Devous, Michael D. and Rabinovici, Gil D. and Alexander, Daniel C. and Lyoo, Chul Hyoung and Evans, Alan C. and Hansson, Oskar}},
issn = {{1078-8956}},
language = {{eng}},
number = {{5}},
pages = {{871--881}},
publisher = {{Nature Publishing Group}},
series = {{Nature Medicine}},
title = {{Four distinct trajectories of tau deposition identified in Alzheimer’s disease}},
url = {{http://dx.doi.org/10.1038/s41591-021-01309-6}},
doi = {{10.1038/s41591-021-01309-6}},
volume = {{27}},
year = {{2021}},
}