CSF markers related to pathogenetic mechanisms in Alzheimer's disease

被引：0

作者：

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

机构：

[1] Departments of Clinical Chemistry,

[2] ,undefined

[3] Neurology,undefined

[4] ,undefined

[5] Pathology,undefined

[6] and,undefined

[7] Psychiatry,undefined

[8] Research Institute Neurosciences,undefined

[9] VU University Medical Center,undefined

[10] Amsterdam,undefined

[11] The Netherlands,undefined

[12] Department of Clinical Neuroscience,undefined

[13] Section of Geriatric Medicine,undefined

[14] Huddinge University Hospital,undefined

[15] Karolinska Institute,undefined

[16] Huddinge,undefined

[17] Sweden,undefined

来源：

Journal of Neural Transmission | 2002年 / 109卷

关键词：

Keywords: C1q; SAP; A-beta (1; 42); tau; pathogenic mechanism.;

D O I：

暂无

中图分类号：

学科分类号：

摘要：

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.

引用

页码：1491 / 1498

页数：7

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