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CSF amyloid β38 as a novel diagnostic marker for dementia with Lewy bodies
  1. Ezra Mulugeta1,2,
  2. Elisabet Londos3,
  3. Clive Ballard2,
  4. Guido Alves4,
  5. Henrik Zetterberg5,
  6. Kaj Blennow5,
  7. Ragnhild Skogseth6,
  8. Lennart Minthon3,
  9. Dag Aarsland1
  1. 1Department of Old Age Psychiatry, Psychiatric Clinic, Stavanger University Hospital, Norway
  2. 2Wolfson Centre for Age Related Diseases, King's College London, London, UK
  3. 3Research Unit, Department of Clinical Sciences, Malmö, University of Lund, Sweden
  4. 4The Norwegian Centre for Movement Disorders, Stavanger University Hospital, Norway
  5. 5Institute of Neuroscience and Physiology, Department of Psychiatry and Neurochemistry, the Sahlgrenska Academy at the University of Gothenburg, Molndal, Sweden
  6. 6Institute of Clinical Medicine, University of Bergen, Norway
  1. Correspondence to Professor D Aarsland, Department of Old Age Psychiatry, Psychiatric Clinic, Stavanger University Hospital, PO Box 8100, N-4068 Stavanger, Norway; daarsland{at}gmail.com

Abstract

Background The clinical distinction between Alzheimer's disease (AD) and dementia with Lewy bodies (DLB) is sometimes difficult, particularly in mild cases. Although CSF markers such as amyloid β42 (Aβ42) and P-tau can distinguish between AD and normal controls, their ability to distinguish between AD and DLB is not adequate.

Objective This study aims to investigate whether CSF markers, in particular levels of Aβ38, can differentiate between mild AD and DLB.

Methods 85 individuals were included after standardised diagnostic procedures: 30 diagnosed as probable AD, 23 probable DLB, 20 probable Parkinson's disease dementia and 12 non-demented control subjects. CSF levels of Aβ38, Aβ40 and Aβ42 were determined using commercially available ultra-sensitive multi-array kit assay (MSD) for human Aβ peptides. Total tau (T-tau) and phosphorylated tau (P-tau) were analysed using ELISA (Innotest). In addition, combinations (Aβ42/Aβ38, Aβ42/Aβ40, Aβ42/P-tau and Aβ42/Aβ38/P-tau) were assessed.

Results Significant between group differences were found for all CSF measures, and all except Aβ40, Aβ42 and Aβ42/P-tau differed between AD and DLB. The Aβ42/Aβ38 ratio was the measure that best discriminated between AD and DLB (AUC 0.765; p<0.005), with a sensitivity of 78% and a specificity of 67%.

Conclusion This study suggests that the level of Aβ38 can potentially contribute in the diagnostic distinction between AD and DLB when combined with Aβ42. Single measures had low diagnostic accuracy, suggesting that developing a panel of markers is the most promising strategy. Studies with independent and larger samples and a priori cut-offs are needed to test this hypothesis.

  • ALZHEIMER'S DISEASE
  • DEMENTIA
  • LEWY BODY
  • PARKINSON'S DISEASE

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Footnotes

  • Funding The study was funded by the Western Norway Regional Health Authority, HelseVest (grant No 911390).

  • Competing interests None.

  • Ethics approval This study was conducted with the approval of the Regional Committee for Medical and Health Research Ethics, Western Norway.

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

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