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Clusterin in cerebrospinal fluid: Analysis of carbohydrates and quantification of native and glycosylated forms
Institute of Clinical Neuroscience, The Sahlgrenska Academy, Göteborg University, Se, 431 80 Mölndal, Sweden.
Discovery Medicine, Molecular Sciences AstraZeneca, Mölndal, Sweden.
Östergötlands Läns Landsting, Local Health Care Services in Central Östergötland, Department of Geriatric Medicine.
Neurotech Department, Section of Clinical Geriatrics, Memoryclinic M 51, Huddinge, SE-141 86 Stockholm, Sweden.
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2006 (English)In: Neurochemistry International, ISSN 0197-0186, E-ISSN 1872-9754, Vol. 48, no 8, 718-728 p.Article in journal (Refereed) Published
Abstract [en]

Clusterin is suggested to be involved in the pathogenesis of Alzheimer's disease. Clusterin expression is increased in brain tissue in affected regions of Alzheimer patients, and intense clusterin staining is found in both senile plaques and in neuronal and glia cells. In contrast, the cerebrospinal fluid level of clusterin in Alzheimer patients has, thus far, been found unchanged. Clusterin is a glycosylated protein, and an alteration of its glycosylation in Alzheimer's disease might influence accurate quantification in cerebrospinal fluid through interference of antibody binding to the protein. Using enzymatic deglycosylation of clusterin isolated from cerebrospinal fluid, we found that the carbohydrates attached to clusterin were of the N-linked type and sialic acids. Based on this finding, cerebrospinal fluid samples from Alzheimer patients (n = 99) and controls (n = 39) were analysed. The samples were treated with peptide: N-glycanase F, cleaving off N-linked carbohydrates, and clusterin was quantified before and after deglycosylation using a new sandwich enzyme-linked immunosorbent assay. Clusterin was significantly increased in Alzheimer patients, in both native (7.17 ± 2.43 AU versus 5.73 ± 2.09 AU, p = 0.002), and deglycosylated samples (12.19 ± 5.00 AU versus 9.68 ± 4.38 AU, p = 0.004). Deglycosylation led to increased measured levels of clusterin by 70% (p < 0.001) in Alzheimer patients and 67% (p < 0.001) in controls. These findings indicate that glycosylation of proteins may interfere with their quantification. The results show that clusterin is significantly increased in cerebrospinal fluid from Alzheimer patients as a group, supporting that clusterin might be involved in the pathogenesis of Alzheimer's disease. However, the individual clusterin levels overlap between the two groups, and thus cerebrospinal fluid clusterin measurement is not suitable as a biochemical marker in the diagnosis of Alzheimer's disease. © 2006 Elsevier Ltd. All rights reserved.

Place, publisher, year, edition, pages
2006. Vol. 48, no 8, 718-728 p.
Keyword [en]
Alzheimer's disease, Carbohydrates, Cerebrospinal fluid
National Category
Natural Sciences
URN: urn:nbn:se:liu:diva-50213DOI: 10.1016/j.neuint.2005.12.005OAI: diva2:271109
Available from: 2009-10-11 Created: 2009-10-11 Last updated: 2010-05-24

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