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Mild behavioral impairment and its relation to tau pathology in preclinical Alzheimer's disease

Johansson, Maurits LU ; Stomrud, Erik LU orcid ; Insel, Philip S. LU ; Leuzy, Antoine LU ; Johansson, Per Mårten LU ; Smith, Ruben LU ; Ismail, Zahinoor ; Janelidze, Shorena LU ; Palmqvist, Sebastian LU orcid and van Westen, Danielle LU orcid , et al. (2021) In Translational Psychiatry 11(1).
Abstract

Mild behavioral impairment (MBI) is suggested as risk marker for neurodegenerative diseases, such as Alzheimer's disease (AD). Recently, pathologic tau deposition in the brain has been shown closely related to clinical manifestations, such as cognitive deficits. Yet, associations between tau pathology and MBI have rarely been investigated. It is further debated if MBI precedes cognitive deficits in AD. Here, we explored potential mechanisms by which MBI is related to AD, this by studying associations between MBI and tau in preclinical AD. In all, 50 amyloid-β-positive cognitively unimpaired subjects (part of the BioFINDER-2 study) underwent MBI-checklist (MBI-C) to assess MBI, and the Alzheimer's Disease Assessment Scale - Cognitive... (More)

Mild behavioral impairment (MBI) is suggested as risk marker for neurodegenerative diseases, such as Alzheimer's disease (AD). Recently, pathologic tau deposition in the brain has been shown closely related to clinical manifestations, such as cognitive deficits. Yet, associations between tau pathology and MBI have rarely been investigated. It is further debated if MBI precedes cognitive deficits in AD. Here, we explored potential mechanisms by which MBI is related to AD, this by studying associations between MBI and tau in preclinical AD. In all, 50 amyloid-β-positive cognitively unimpaired subjects (part of the BioFINDER-2 study) underwent MBI-checklist (MBI-C) to assess MBI, and the Alzheimer's Disease Assessment Scale - Cognitive subscale (ADAS-Cog) delayed word recall (ADAS-DR) to assess episodic memory. Early tau pathology was determined using tau-PET ([18F]RO948 retention in entorhinal cortex/hippocampus) and cerebrospinal fluid (CSF) P-tau181. Regression models were used to test for associations. We found that higher tau-PET signal in the entorhinal cortex/hippocampus and CSF P-tau181 levels were associated with higher MBI-C scores (β = 0.010, SE = 0.003, p = 0.003 and β = 1.263, SE = 0.446, p = 0.007, respectively). When MBI-C and ADAS-DR were entered together in the regression models, tau-PET (β = 0.009, p = 0.009) and CSF P-tau181 (β = 0.408, p = 0.006) were predicted by MBI-C, but not ADAS-DR. We conclude that in preclinical AD, MBI is associated with tau independently from memory deficits. This denotes MBI as an important early clinical manifestation related to tau pathology in AD.

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type
Contribution to journal
publication status
published
subject
in
Translational Psychiatry
volume
11
issue
1
article number
76
publisher
Nature Publishing Group
external identifiers
  • pmid:33500386
  • scopus:85099860453
ISSN
2158-3188
DOI
10.1038/s41398-021-01206-z
language
English
LU publication?
yes
id
acd26f7d-e9da-40a2-ab14-732223540080
date added to LUP
2021-02-03 09:42:51
date last changed
2024-06-13 06:33:27
@article{acd26f7d-e9da-40a2-ab14-732223540080,
  abstract     = {{<p>Mild behavioral impairment (MBI) is suggested as risk marker for neurodegenerative diseases, such as Alzheimer's disease (AD). Recently, pathologic tau deposition in the brain has been shown closely related to clinical manifestations, such as cognitive deficits. Yet, associations between tau pathology and MBI have rarely been investigated. It is further debated if MBI precedes cognitive deficits in AD. Here, we explored potential mechanisms by which MBI is related to AD, this by studying associations between MBI and tau in preclinical AD. In all, 50 amyloid-β-positive cognitively unimpaired subjects (part of the BioFINDER-2 study) underwent MBI-checklist (MBI-C) to assess MBI, and the Alzheimer's Disease Assessment Scale - Cognitive subscale (ADAS-Cog) delayed word recall (ADAS-DR) to assess episodic memory. Early tau pathology was determined using tau-PET ([18F]RO948 retention in entorhinal cortex/hippocampus) and cerebrospinal fluid (CSF) P-tau181. Regression models were used to test for associations. We found that higher tau-PET signal in the entorhinal cortex/hippocampus and CSF P-tau181 levels were associated with higher MBI-C scores (β = 0.010, SE = 0.003, p = 0.003 and β = 1.263, SE = 0.446, p = 0.007, respectively). When MBI-C and ADAS-DR were entered together in the regression models, tau-PET (β = 0.009, p = 0.009) and CSF P-tau181 (β = 0.408, p = 0.006) were predicted by MBI-C, but not ADAS-DR. We conclude that in preclinical AD, MBI is associated with tau independently from memory deficits. This denotes MBI as an important early clinical manifestation related to tau pathology in AD.</p>}},
  author       = {{Johansson, Maurits and Stomrud, Erik and Insel, Philip S. and Leuzy, Antoine and Johansson, Per Mårten and Smith, Ruben and Ismail, Zahinoor and Janelidze, Shorena and Palmqvist, Sebastian and van Westen, Danielle and Mattsson-Carlgren, Niklas and Hansson, Oskar}},
  issn         = {{2158-3188}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{1}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Translational Psychiatry}},
  title        = {{Mild behavioral impairment and its relation to tau pathology in preclinical Alzheimer's disease}},
  url          = {{http://dx.doi.org/10.1038/s41398-021-01206-z}},
  doi          = {{10.1038/s41398-021-01206-z}},
  volume       = {{11}},
  year         = {{2021}},
}