Alzheimer CSF biomarkers in routine clinical setting

Authors


M. Rigaud, ASTRALAB, 7-11 Avenue de Lattre de Tassigny, 87000 Limoges, France
Tel.: 00 33 5 55 30 29 30
Fax: 00 33 5 55 48 85 01
e-mail: rigaud.michel@ yahoo.fr.

Abstract

Tabaraud F, Leman JP, Milor AM, Roussie JM, Barrière G, Tartary M, Boutros-Toni F, Rigaud M. Alzheimer CSF biomarkers in routine clinical setting.
Acta Neurol Scand: 2012: 125: 416–423.
© 2011 John Wiley & Sons A/S.

Objectives –  Our work was aimed to evaluate Alzheimer’s disease diagnosis improvement using cerebrospinal fluid biomarkers (CSF) in neurological daily practice.

Materials and Methods –  For this purpose, 150 patients clinically and neurochemically classified as having AD or cognitive impairment with or without other dementia type were included in the study. The following CSF peptides were studied, blindly to the clinical diagnosis: beta-amyloid1–42 peptide (Aβ1–42), Tau (T-tau), threonine-181 hyperphosphorylated tau protein (P-tau181), and beta-amyloid1–40 peptide (Aβ1–40). From these measurements, Innotest® Amyloid Tau Index (IATI) was calculated for each patient.

Results –  This assessment allowed to separate 83 biochemical profiles of AD and 67 non-Alzheimer’s disease (non-AD), both AD and non-AD categories match with clinical data amounting to 73% and 90%, respectively. Among mild cognitive impairment (MCI) patients, CSF biomarkers led to discriminate those who are likely to be AD. We devoted a special section to Aβ1–40 which is not a routine parameter but can help to confirm a pathological amyloid process as Aβ1–42/Aβ1–40 ratio underlining the real decline of the Aβ1–42.

Conclusions –  The interest of biomarkers and their ability to solve awkward cases were carefully noticed all the more when a discrepancy between clinical and CSF biological data was involved. The final proposed algorithm allowed to identify pathogenic forms of AD according to the prevailing role of hyperphosphorylated tau or amyloid beta peptide.

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