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Relevance of the interplay between amyloid and tau for cognitive impairment in early Alzheimer's disease.

Journal article
Authors Maarten Timmers
Ina Tesseur
Jennifer Bogert
Henrik Zetterberg
Kaj Blennow
Anne Börjesson-Hanson
Miquel Baquero
Mercè Boada
Christopher Randolph
Luc Tritsmans
Luc Van Nueten
Sebastiaan Engelborghs
Johannes Rolf Streffer
Published in Neurobiology of aging
Volume 79
Pages 131-141
ISSN 1558-1497
Publication year 2019
Published at Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry
Centre for Ageing and Health (Agecap)
Pages 131-141
Language en
Subject categories Neurochemistry


Amyloid β (Aβ) and tau are key hallmark features of Alzheimer's disease (AD) neuropathology. The interplay of Aβ and tau for cognitive impairment in early AD was examined with cross-sectional analysis, measured by cerebrospinal fluid biomarkers (Aβ1-42, total tau [t-tau], and phosphorylated tau [p-tau181P]), and on cognitive performance by the repeatable battery for assessment of neuropsychological status (RBANS). Participants (n = 246) included cognitively normal (Aβ-), mild cognitively impaired (Aβ-), preclinical AD (Aβ+), and prodromal AD (Aβ+). Overall, cognitive scores (RBANS total scale score) had a moderate negative correlation to t-tau (n = 246; r = -0.434; p < 0.001) and p-tau181P (r = -0.389; p < 0.001). When classified by Aβ status, this correlation to t-tau was applicable only in Aβ+ participants (n = 139; r = -0.451, p < 0.001) but not Aβ- participants (n = 107; r = 0.137, p = 0.16), with identical findings for p-tau. Both tau (p < 0.0001) and interaction of Aβ1-42 with tau (p = 0.006) affected RBANS, but not Aβ1-42 alone. Cognitive/memory performance correlated well with cerebrospinal fluid tau levels across early stages of AD, although the correlation is Aβ dependent.

Page Manager: Webmaster|Last update: 9/11/2012

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