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Fluid biomarker agreement and interrelation in dementia due to Alzheimer’s disease

  • Psychiatry and Preclinical Psychiatric Studies - Original Article
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Abstract

The cerebrospinal fluid (CSF) levels of β-amyloid 42, total tau, and phosphorylated tau 181 are supposed to be all continuously abnormal in dementia due to Alzheimer’s disease (AD), being the most advanced disease stage. The aim of the present study, which included a monocentric and a multicentric sample (N = 119 and 178, respectively), was to investigate the degree of CSF biomarker agreement and interrelation in AD dementia. Based on previously published cut-off values, biomarker values were categorized as positive or negative for AD (dichotomization strategy) and as either positive, negative, or borderline (trichotomization strategy). The statistical analyses relied on distance correlation analysis and kappa (k) statistics. Poor agreement (k < 0.4) and low interrelations between the studied biomarkers were detected in all cases with the exception of the interrelation between the markers total tau and phosphorylated tau 181, especially in the monocentric sample. Interestingly, lower interrelation and agreement degrees were observed in carriers of the Apolipoprotein E ε4 allele compared to non-carriers. The clinical phenotype currently referred to as “AD dementia” is characterized by an inhomogeneous CSF biomarker profile, possibly mirroring the complex genesis of AD-typical dementia symptoms and pointing to the necessity of shedding more light on the hypothesis of biomarker stability over time in symptomatic AD.

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Acknowledgements

Data collection and sharing for this project were funded by the Alzheimer’s Disease Neuroimaging Initiative (ADNI) (National Institutes of Health Grant U01 AG024904) and DOD ADNI (Department of Defense award number W81XWH-12-2-0012). ADNI is funded by the National Institute on Aging, the National Institute of Biomedical Imaging and Bioengineering, and through generous contributions from the following: AbbVie, Alzheimer’s Association; Alzheimer’s Drug Discovery Foundation; Araclon Biotech; BioClinica, Inc.; Biogen; Bristol-Myers Squibb Company; CereSpir, Inc.; Cogstate; Eisai Inc.; Elan Pharmaceuticals, Inc.; Eli Lilly and Company; EuroImmun; F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc.; Fujirebio; GE Healthcare; IXICO Ltd.; Janssen Alzheimer Immunotherapy Research & Development, LLC.; Johnson & Johnson Pharmaceutical Research & Development LLC.; Lumosity; Lundbeck; Merck & Co., Inc.; Meso Scale Diagnostics, LLC.; NeuroRx Research; Neurotrack Technologies; Novartis Pharmaceuticals Corporation; Pfizer Inc.; Piramal Imaging; Servier; Takeda Pharmaceutical Company; and Transition Therapeutics. The Canadian Institutes of Health Research is providing funds to support ADNI clinical sites in Canada. Private sector contributions are facilitated by the Foundation for the National Institutes of Health (http://www.fnih.org). The grantee organization is the Northern California Institute for Research and Education, and the study is coordinated by the Alzheimer’s Therapeutic Research Institute at the University of Southern California. ADNI data are disseminated by the Laboratory for Neuro Imaging at the University of Southern California.

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  1. Panagiotis Alexopoulos and Jennifer Roesler have contributed equally.

Authors and Affiliations

  1. Department of Psychiatry, University of Patras, 26500, Rion Patras, Greece

    Panagiotis Alexopoulos, Iliana Lentzari & Philippos Gourzis

  2. Department of Psychiatry and Psychotherapy, Technical University of Munich, Ismaninger Str. 22, 81675, Munich, Germany

    Panagiotis Alexopoulos, Jennifer Roesler, Lukas Werle, Nathalie Thierjung, Marion Ortner, Timo Grimmer & Alexander Kurz

  3. Max Planck Institute of Psychiatry, Munich, Germany

    Lukas Werle

  4. Department of Informatics, Aristotle University of Thessaloniki, 54124, Thessaloniki, Greece

    Nikolaos Laskaris

  5. First Department of Psychiatry, Eginition Hospital, National and Kapodistrian University of Athens, Vassilissis Sofias Ave 72-74, 11528, Athens, Greece

    Antonios Politis

  6. Division of Geriatric Psychiatry and Neuropsychiatry, Department of Psychiatry, John’s Hopkins Medical School, Baltimore, USA

    Antonios Politis

  7. Department of Psychiatry and Psychotherapy, Ludwig-Maximilians-Universität München, Nussbaumstraße 7, 80336, Munich, Germany

    Robert Perneczky

  8. Neuroepidemiology and Ageing Research Unit, School of Public Health, Faculty of Medicine, The Imperial College of Science, Technology and Medicine, London, UK

    Robert Perneczky

  9. West London Mental Health NHS Trust, London, UK

    Robert Perneczky

  10. German Center for Neurodegenerative Diseases (DZNE) Munich, Munich, Germany

    Robert Perneczky

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  1. Panagiotis Alexopoulos
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  2. Jennifer Roesler
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For the Alzheimer’s Disease Neuroimaging Initiative

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Correspondence to Panagiotis Alexopoulos.

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The authors declare no competing financial interest.

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All procedures performed in the study were in accordance with the ethical standards of the institutional research committees and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.

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Informed consent was obtained from all individual participants included in the study.

Additional information

Data used in preparation of this article were obtained from the Alzheimer’s Disease Neuroimaging Initiative (ADNI) database (http://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf.

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Alexopoulos, P., Roesler, J., Werle, L. et al. Fluid biomarker agreement and interrelation in dementia due to Alzheimer’s disease. J Neural Transm 125, 193–201 (2018). https://doi.org/10.1007/s00702-017-1810-z

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