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Neurobiol Aging. 2019 Apr 1;79:131-141. doi: 10.1016/j.neurobiolaging.2019.03.016. [Epub ahead of print]

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

Author information

1
Janssen Research and Development, A Division of Janssen Pharmaceutica N.V., Beerse, Belgium; Reference Center for Biological Markers of Dementia (BIODEM), Institute Born-Bunge, University of Antwerp, Antwerp, Belgium. Electronic address: mtimmer3@its.jnj.com.
2
Janssen Research and Development, A Division of Janssen Pharmaceutica N.V., Beerse, Belgium.
3
Janssen Research and Development LLC, Raritan, NJ, USA.
4
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistery Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden; Department of Neurodegenerative Disease, UCL Institute of Neurology, Queen Square, London, UK; UK Dementia Research Institute at UCL, London, UK.
5
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Clinical Neurochemistery Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
6
Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden; Sahlgrenska University Hospital, Mölndal, Sweden; Clinical Trials, Theme Aging, Karolinska University Hospital, Stockholm, Sweden.
7
Neurology Department, Hospital Universitari I Politecnic La Fe, Valencia, Spain.
8
Research Center and Memory Clinic, Fundació ACE, Institut Català de Neurociències Aplicades, Universitat Internacional de Catalunya-Barcelona, Spain; Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Instituto de Salud Carlos III, Madrid, Spain.
9
MedAvante-ProPhase, Hamilton, NJ, USA; Department of Neurology, Loyola University Medical Center, Maywood, IL, USA.
10
Reference Center for Biological Markers of Dementia (BIODEM), Institute Born-Bunge, University of Antwerp, Antwerp, Belgium; Department of Neurology and Center for Neurosciences, UZ Brussel and Vrije Universiteit Brussel (VUB), Brussels, Belgium.
11
Janssen Research and Development, A Division of Janssen Pharmaceutica N.V., Beerse, Belgium; Reference Center for Biological Markers of Dementia (BIODEM), Institute Born-Bunge, University of Antwerp, Antwerp, Belgium.

Abstract

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.

KEYWORDS:

Alzheimer’s disease; Amyloid; Cognition; Interaction; RBANS; Tau

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