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Differences and Similarities between Two Frequently Used Assays for Amyloid ß 42 in Cerebrospinal Fluid

¹ Alzheimer Center and Department of Neurology, and² Department of Clinical Chemistry, VU University Medical Center, Amsterdam, The Netherlands;³ Innogenetics NV, Ghent, Belgium;⁴ Institute for Basic Research in Developmental Disabilities, Department of Developmental Neurobiology, Division of Immunology, Staten Island, NY;

^aaddress correspondence to this author at: Departments of Neurology and Clinical Chemistry, VU University Medical Center, PO Box 7057, 1081 HV Amsterdam, The Netherlands; fax 31-(0)204440715, e-mail niki.schoonenboom@vumc.nl

The first 300 words of the full text of this article appear below.

Amyloid ß 42 (Aß 42) concentrations in cerebrospinal fluid (CSF) are used to identify Alzheimer disease (AD) (1), but reported concentrations differ among studies, as does diagnostic accuracy (2). These differences may relate to the patient and control groups studied (3), processing and storage methods (4), intra- and interassay variation of the assays, or to the reagent antibodies used. A recent metaanalysis (2) stressed the importance of standardizing assays for Aß–42 in CSF. In most studies, CSF Aß 42 was reported to be decreased, but in 2 studies, CSF Aß 42 was not significantly changed in AD (2), and in 1 study(5) even increased in the early stages of disease. These dissimilarities might reflect the specificities of the antibodies incorporated in the assays.

The first aim of our study was to compare Aß 42 concentrations measured by 2 different assays in the same CSF samples. The first assay, widely used in Europe (6), uses 2 monoclonal antibodies (mAbs) and detects the full-length Aß 42 peptide, Aß (1–42) (7). The second assay [Aß (N–42)], used mainly in the United States (8), detects both full-length Aß 42 and Aß peptides truncated at the NH₂ terminus (9).

The second aim of our study was to compare diagnostic accuracies of the assays for patients with AD compared with controls without dementia and patients with frontotemporal lobar degeneration (FTLD).

Finally, we investigated the relationship between CSF Aß (1–42) and Aß (N–42) concentrations and albumin ratio, age, disease duration, and disease severity.

Between October 2000 and December 2002, we recruited 39 AD patients, 24 FTLD patients, and 30 non-dementia controls at the Alzheimer Center of the VU University Medical Center (VUMC). All patients underwent . . . [Full Text of this Article]