Aβ38 and Aβ43 do not differentiate between Alzheimer's disease and cerebral amyloid angiopathy

Author:

Dargvainiene Justina1ORCID,Jensen‐Kondering Ulf23ORCID,Bender Benjamin4,Berg Daniela56,Brüggemann Norbert7,Flüh Charlotte8,Markewitz Robert1,Neumann Alexander2,Röben Benjamin69ORCID,Röcken Christoph9,Royl Georg7,Schulte Claudia610,Wandinger Klaus‐Peter1,Weiler Caroline5,Margraf Nils G.5ORCID,Kuhlenbäumer Gregor5ORCID

Affiliation:

1. Institute of Clinical Chemistry University Medical Center Schleswig‐Holstein, Campus Kiel Kiel Germany

2. Department of Neuroradiology University Medical Center Schleswig‐Holstein, Campus Lübeck Lübeck Germany

3. Department of Radiology and Neuroradiology University Medical Center Schleswig‐Holstein, Campus Kiel, Kiel University (CAU) Kiel Germany

4. Department of Radiology, Diagnostical and Interventional Neuroradiology University Hospital of Tübingen Tübingen Germany

5. Department of Neurology University Medical Center Schleswig‐Holstein, Campus Kiel, Kiel University (CAU) Kiel Germany

6. Department of Neurodegeneration, Hertie Institute for Clinical Brain Research University of Tübingen Tübingen Germany

7. Department of Neurology University Medical Center Schleswig‐Holstein, Campus Lübeck Lübeck Germany

8. Department of Neurosurgery University Medical Center Schleswig‐Holstein, Campus Kiel, Kiel University (CAU) Kiel Germany

9. Department of Pathology University Medical Center Schleswig‐Holstein, Campus Kiel, Kiel University (CAU) Kiel Germany

10. German Center for Neurodegenerative Diseases University of Tübingen Tübingen Germany

Abstract

AbstractDifferential diagnosis between Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA) using cerebrospinal fluid (CSF) biomarkers is challenging. A recent study suggested that the addition of Aβ38 and Aβ43 to a standard AD biomarker panel (Aβ40, Aβ42, t‐tau, p‐tau) to improve the differential diagnosis. We tested this hypothesis in an independent German cohort of CAA and AD patients and controls using the same analytical techniques. We found excellent discrimination between AD and controls and between CAA and controls, but not between AD and CAA. Adding Aβ38 and Aβ43 to the panel did not improve the discrimination between AD and CAA.

Publisher

Wiley

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