Plasma amyloid is associated with the rate of cognitive decline in cognitively normal elderly: the SCIENCe project.


Journal

Neurobiology of aging
ISSN: 1558-1497
Titre abrégé: Neurobiol Aging
Pays: United States
ID NLM: 8100437

Informations de publication

Date de publication:
05 2020
Historique:
received: 07 06 2019
revised: 12 12 2019
accepted: 13 01 2020
pubmed: 23 2 2020
medline: 24 9 2020
entrez: 22 2 2020
Statut: ppublish

Résumé

Plasma biomarkers are promising prognostic tools in individuals with subjective cognitive decline (SCD). We aimed to investigate the relationships of baseline plasma amyloid beta (Aβ)42/Aβ40 and total Tau (tTau) with rate of cognitive decline, in comparison to relationships of baseline cerebrospinal fluid (CSF) Aβ42, tTau, and phosphorylated tau181 (pTau181) with rate of cognitive decline. We included 241 subjects with SCD (age = 61 ± 9, 40% female, Mini-Mental State Examination = 28 ± 2) with follow-up (average: 2 ± 2 years, median visits: 3 [range: 1-11]) for re-evaluation of neuropsychological test performance (attention, memory, language, and executive functioning domains). Using age, gender and education-adjusted linear mixed models, we found that lower plasma Aβ42/Aβ40 was associated with steeper rate of decline on tests for attention, memory, and executive functioning, but not language. Lower CSF Aβ42 was associated with steeper decline on tests covering all domains. Associations for plasma amyloid and cognitive decline mirror those of CSF amyloid. Plasma tTau was not associated with rate of cognitive decline, whereas CSF tTau and pTau181 were on multiple tests covering all domains.

Identifiants

pubmed: 32081465
pii: S0197-4580(20)30015-4
doi: 10.1016/j.neurobiolaging.2020.01.007
pii:
doi:

Substances chimiques

Amyloid beta-Peptides 0
Biomarkers 0
Peptide Fragments 0
amyloid beta-protein (1-42) 0
amyloid beta-protein (40-42) 0
tau Proteins 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

99-107

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Auteurs

Inge M W Verberk (IMW)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands; Neurochemistry Laboratory, Department of Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands. Electronic address: i.verberk@amsterdamumc.nl.

Heleen M A Hendriksen (HMA)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Argonde C van Harten (AC)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Linda M P Wesselman (LMP)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Sander C J Verfaillie (SCJ)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Karlijn A van den Bosch (KA)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Rosalinde E R Slot (RER)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Niels D Prins (ND)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Philip Scheltens (P)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Charlotte E Teunissen (CE)

Neurochemistry Laboratory, Department of Clinical Chemistry, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

Wiesje M Van der Flier (WM)

Alzheimer Center, Department of Neurology, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands; Department of Epidemiology and Biostatistics, Vrije Universiteit Amsterdam, Amsterdam UMC, Amsterdam, the Netherlands.

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Classifications MeSH