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Amyloid-β peptides in cerebrospinal fluid of patients with dementia with Lewy bodies

  • van Steenoven, Inger1
  • van der Flier, Wiesje M.1, 2
  • Scheltens, Philip1
  • Teunissen, Charlotte E.3
  • Lemstra, Afina W.1
  • 1 Vrije Universiteit Amsterdam, Amsterdam UMC, Alzheimer Center Amsterdam, Department of Neurology, Amsterdam Neuroscience, De Boelelaan 1118, Amsterdam, 1081 HV, The Netherlands , Amsterdam (Netherlands)
  • 2 Vrije Universiteit Amsterdam, Amsterdam UMC, Department of Epidemiology and Biostatistics, Amsterdam Neuroscience, Amsterdam, The Netherlands , Amsterdam (Netherlands)
  • 3 Vrije Universiteit Amsterdam, Amsterdam UMC, Neurochemistry Laboratory and Biobank, Department of Clinical Chemistry, Amsterdam Neuroscience, Amsterdam, The Netherlands , Amsterdam (Netherlands)
Published Article
Alzheimer's Research & Therapy
BioMed Central
Publication Date
Oct 10, 2019
DOI: 10.1186/s13195-019-0537-5
Springer Nature


BackgroundOne of the major challenges in diagnosing dementia with Lewy bodies (DLB) is the common co-morbid presence of amyloid pathology. To understand the putative role of altered amyloid-β (Aβ) metabolism in dementia with DLB, we analyzed levels of different cerebrospinal fluid (CSF) Aβ peptides (Aβ38, Aβ40, Aβ42) in DLB, Alzheimer’s disease (AD), and cognitively normal controls.MethodsCSF from patients with DLB (n = 72; age 68 ± 6 years; 10%F; Mini-mental State examination (MMSE) 23 ± 4), AD (n = 38; age 68 ± 6 years; 8%F; MMSE 22 ± 5), and cognitively normal controls (n = 38; age 67 ± 7 years; 13%F; MMSE 29 ± 2) was analyzed using the Meso Scale Discovery assay for human Aβ peptides. We performed general linear models to compare CSF Aβ peptide levels between groups. Associations between CSF Aβ peptides and MMSE score at baseline and longitudinal changes over time were assessed with linear mixed models.ResultsFor all three CSF Aβ peptides and compared to controls (Aβ38 2676 ± 703 pg/ml, Aβ40 6243 ± 1500 pg/ml, and Aβ42 692 ± 205 pg/ml), we observed lower levels in DLB (Aβ38 2247 ± 638, Aβ40 5432 ± 1340, and Aβ42 441 ± 185, p < 0.05), whereas AD patients showed only lower Aβ42 levels (304 ± 71, p < 0.001). The observed differences in Aβ38 and Aβ40 were independent of co-morbid AD pathology (CSF tau/Aβ42 > 0.52) and APOE genotype. Finally, lower Aβ peptide levels were associated with lower MMSE score (β = 1.02–1.11, p < 0.05).ConclusionWe demonstrated different profiles of CSF Aβ reduction in DLB and AD. In particular, while AD is characterized by an isolated drop in Aβ42, DLB comes with reductions in Aβ38, Aβ40, and Aβ42. This suggests that amyloid metabolism is affected in DLB, even in the absence of co-morbid AD pathology.

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