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EMBO Mol Med. 2017 Sep;9(9):1212-1223. doi: 10.15252/emmm.201707809.

18F-AV-1451 and CSF T-tau and P-tau as biomarkers in Alzheimer's disease.

Author information

1
Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden niklas.mattsson@med.lu.se oskar.hansson@med.lu.se.
2
Memory Clinic, Skåne University Hospital, Lund, Sweden.
3
Department of Neurology, Skåne University Hospital, Lund, Sweden.
4
Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden.
5
MedTech West and the Department of Psychiatry and Neurochemistry, University of Gothenburg, Gothenburg, Sweden.
6
Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, San Francisco, CA, USA.
7
Department of Radiology and Biomedical Imaging, University of California, San Francisco, CA, USA.
8
Department of Clinical Neurophysiology, Skåne University Hospital, Lund, Sweden.
9
Department of Radiation physics, Skåne University Hospital, Lund, Sweden.
10
Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Mölndal, Sweden.
11
Department of Molecular Neuroscience, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Mölndal, Sweden.
12
Department of Molecular Neuroscience, UCL Institute of Neurology, London, UK.
13
Department of Clinical Physiology and Nuclear Medicine, Skåne University Hospital, Lund, Sweden.

Abstract

To elucidate the relationship between cerebrospinal fluid (CSF) total-tau (T-tau) and phosphorylated tau (P-tau) with the tau PET ligand 18F-AV-1451 in Alzheimer's disease (AD), we examined 30 cognitively healthy elderly (15 with preclinical AD), 14 prodromal AD, and 39 AD dementia patients. CSF T-tau and P-tau were highly correlated (R = 0.92, P < 0.001), but they were only moderately associated with retention of 18F-AV-1451, and mainly in demented AD patients. 18F-AV-1451, but not CSF T-tau or P-tau, was strongly associated with atrophy and cognitive impairment. CSF tau was increased in preclinical AD, despite normal 18F-AV-1451 retention. However, not all dementia AD patients exhibited increased CSF tau, even though 18F-AV-1451 retention was always increased at this disease stage. We conclude that CSF T-tau and P-tau mainly behave as biomarkers of "disease state", since they appear to be increased in many cases of AD at all disease stages, already before the emergence of tau aggregates. In contrast, 18F-AV-1451 is a biomarker of "disease stage", since it is increased in clinical stages of the disease, and is associated with brain atrophy and cognitive decline.

KEYWORDS:

Alzheimer; biomarker; cerebrospinal fluid; positron emission tomography; tau

PMID:
28743782
PMCID:
PMC5582410
DOI:
10.15252/emmm.201707809
[Indexed for MEDLINE]
Free PMC Article

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