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International Journal of Alzheimer’s Disease
Volume 2011 (2011), Article ID 495025, 6 pages
Clinical Study

Cerebrospinal Fluid Levels of sAPPα and sAPPβ in Lewy Body and Alzheimer's Disease: Clinical and Neurochemical Correlates

1Centre for Age-Related Medicine, Stavanger University Hospital, 4068 Stavanger, Norway
2Wolfson Centre for Age-Related Diseases, King's College London, London SE1 1UL, UK
3Research Unit, Department of Clinical Sciences, Malmö, University of Lund, Lund, Norway
4Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy, University of Gothenburg, Molndal, Gothenburg, Sweden
5NVS Department, KI Alzheimer Disease Research Center, Karolinska Institutet, Novum, 14186 Stockholm, Sweden
6Institute of Clinical Medicine, Akershus University Hospital, University of Oslo, Oslo, Norway

Received 7 April 2011; Revised 13 June 2011; Accepted 19 July 2011

Academic Editor: Lucilla Parnetti

Copyright © 2011 Ezra Mulugeta et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We measured cerebrospinal fluid (CSF) levels of the soluble isoforms of amyloid precursor protein (APP; sAPPα sAPPβ) and other CSF biomarkers in 107 patients with Alzheimer's disease (AD), dementia with Lewy body dementia (DLB), Parkinson's disease dementia (PDD), and normal controls (NC) using commercial kits. DLB and PDD were combined in a Lewy body dementia group (LBD). No differences were observed in sAPPα and sAPPβ levels between the groups. Significant correlations were observed between sAPPα and sAPPβ and between sAPPβ and Mini-Mental State Examination scores in the total group analysis as well as when LBD and AD groups were analyzed separately. sAPPα and sAPPβ levels correlated with Aβ38, Aβ40, Aβ42, and Tau in the LBD group. In AD, sAPPα correlated with p-Tau and sAPPβ with Aβ40. The differential association between sAPPα and sAPPβ with Aβ and Tau species between LBD and AD groups suggests a possible relationship with the underlying pathologies in LBD and AD.