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CSF tau proteins correlate with an atypical clinical presentation in dementia with Lewy bodies
  1. Rita Di Censo1,
  2. Carla Abdelnour2,
  3. Frederic Blanc3,4,
  4. Olivier Bousiges5,
  5. Afina W Lemstra6,
  6. Inger van Steenoven7,
  7. Marco Onofrj1,8,
  8. Dag Aarsland8,9,
  9. Laura Bonanni1,10
  10. on behalf of the European DLB consortium
    1. 1 Department of Neuroscience, Imaging and Clinical Sciences, University Chieti-Pescara, Institute of Neurology, Chieti, Italy
    2. 2 Department of Medicine of the Universitat Autònoma de Barcelona, Barcelona, Spain. Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas (CIBERNED), Research Center and Memory Clinic of Fundació ACE, Institut Català de Neurociències Aplicades, Univesitat Internacional de Catalunya, Barcelona, Spain, Barcelona, Spain
    3. 3 Neurology, University Hospital of Strasbourg, strasbourg, France
    4. 4 ICube, University of Strasbourg and CNRS, Strabsourg, France
    5. 5 Laboratoire de biochimie et biologie moléculaire, Hôpital de Hautepierre, Strasbourg, France
    6. 6 Neurology, VU University Medical Center, Amsterdam, The Netherlands
    7. 7 Neurology/Alzheimercenter, VU University Medical Center, Amsterdam, The Netherlands
    8. 8 Department of Old Age Psychiatry, Institute of Psychiatry, Psychology and Neuroscience, King’s College, London, UK
    9. 9 Center for Age related Medicine, Stavanger University Hospital, Stavanger, Norway
    10. 10 CeSI, University Foundation, Aging Research Center, Chieti, Italy
    1. Correspondence to Laura Bonanni, Department of Neuroscience, Imaging and Clinical Sciences, University Chieti-Pescara, Institute of Neurology, Chieti, IT 66100, Italy; l.bonanni{at}

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    A cerebrospinal fluid (CSF) Alzheimer’s disease (AD) profile, that is, decreased amyloid-β1-42 (Aβ42) and increased total tau protein (t-tau) and/or phosphorylated tau at threonine-181 (p-tau),1 has been identified in a substantial number of dementia with Lewy bodies (DLB) patients, and it has been related to a more rapid cognitive decline.1 We investigated the association between AD CSF biomarkers and DLB core clinical features to better understand in vivo how AD pathology influences DLB clinical presentation.

    We included 171 subjects with a clinical diagnosis of probable DLB2 3 from the European DLB consortium (E-DLB). The centres involved are summarised in online supplementary table 1. Clinical examination was performed as previously reported.1 Dopamine transporter (DAT) single-photon emission CT scans (123I-FP-CIT-SPECT) were performed in 80 patients.

    Supplemental material


    CSF samples were collected at each centre according to the procedures detailed in online supplementary table 1. An AD CSF profile was defined as low Aβ42 combined with high t-tau or p-tau.1 Information about pharmacological treatments of patients were not available at each centre. Statistical analyses were performed using SPSS V.24. Association between CSF biomarkers (normal or abnormal), and each core features (present or absent), were tested with χ2 test. Associations between single CSF biomarkers and groups of subjects with different core clinical features’ number (1–4) were tested with Armitage test for trend.

    Local ethics committees approved the study. All patients gave their written consent for the use of their …

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    • Collaborators Angelo Antonini, Clive Ballard, Claudio Babiloni, Alexandra Bernadotte, Roberta Biundo, Bradly Boeve, Jan Booij, Sevasti Bostantjopoulou, Carlo De Lena, Richard Dodel, Cristian Falup-Pecurariu,Tormod Fladby, Sara Garcia- Pacek, Josep Garre, Gert J. Geurtsen, Martha Therese Gjestsen, Oskar Hansson, Frank Jan de Jong, Vesna Jelic, Zoe Katsarou, Milica Kramberger, Elisabet Londos, Ian McKeith, Brit Mollenhauer, Flavio Nobili, John O’Brien, Alessandro Padovani, Maria Petrova, Andrea Pilotto, Irena Rektorova, Arvid Rongve, Jon Snaedal, Elka Stefanova, Per Svenningsson, John Paul Taylor, Pietro Tiraboschi, Latchezar Traykov, Rik Vandenberghe, Zuzana Walker, Eric Westman, Bengt Winblad, Henrik Zetterberg.

    • Contributors RDC analysed the data, performed statistical analyses and wrote the manuscript. CA, FB, OB, AWL, IvS provided CSF data and critically revised the paper; MO critically revised the paper, DA and LB supervised RDC work and critically revised the manuscript.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Provenance and peer review Not commissioned; externally peer reviewed.