CSF markers related to pathogenetic mechanisms in Alzheimer's disease

C. Mulder, S. N.M. Schoonenboom, L. O. Wahlund, Ph Scheltens, G. J. Van Kamp*, R. Veerhuis, C. E. Hack, M. Blomberg, R. B.H. Schutgens, P. Eikelenboom

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review


Serum amyloid P component (SAP) and complement C1q are found highly co-localized with extracellular fibrillar amyloidβ (Aβ) deposits in Alzheimer's disease (AD) brain. Conflicting data were reported earlier about the cerebrospinal fluid (CSF) levels of SAP and C1q in AD compared to controls. The objective of the present study was to compare the levels of Aβ1-42, tau, C1q and SAP in CSF of a well characterized group of AD patients and controls, and to assess the association with dementia severity. Significantly decreased CSF levels of Aβ1-42 were observed in the AD group (480 ± 104ng/L) as compared to controls (1,040 ± 213ng/L), whereas tau levels were significantly higher in patients with AD (618 ± 292ng/L) than in controls (277 ± 136ng/L). Combining the results of Aβ1-42 and tau measurements resulted in a clear separation between the AD group and the controls. No significant differences in CSF levels of SAP and C1q were observed between the well characterized AD patients and non demented control group. Furthermore, we could not demonstrate a correlation between SAP and C1q CSF levels and the severity of the disease, expressed in Mini-Mental State Examination (MMSE) scores. Therefore, in our opinion these factors can be excluded from the list of potentially interesting biomarkers for AD diagnosis and progression.

Original languageEnglish
Pages (from-to)1491-1498
Number of pages8
JournalJournal of Neural Transmission
Issue number12
Publication statusPublished - 1 Dec 2002

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