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Measurement of phosphorylated tau epitopes in the differential diagnosis of Alzheimer disease: a comparative cerebrospinal fluid study.

Artikel i vetenskaplig tidskrift
Författare Harald Hampel
Katharina Buerger
Raymond Zinkowski
Stefan J Teipel
Alexander Goernitz
Niels Andreasen
Magnus Sjoegren
John DeBernardis
Daniel Kerkman
Koichi Ishiguro
Hideto Ohno
Eugeen Vanmechelen
Hugo Vanderstichele
Cheryl McCulloch
Hans-Jurgen Moller
Peter Davies
Kaj Blennow
Publicerad i Archives of general psychiatry
Volym 61
Nummer/häfte 1
Sidor 95-102
ISSN 0003-990X
Publiceringsår 2004
Publicerad vid Institutionen för laboratoriemedicin, Avdelningen för klinisk kemi/transfusionsmedicin
Sidor 95-102
Språk en
Länkar dx.doi.org/10.1001/archpsyc.61.1.95
Ämnesord Aged, Aged, 80 and over, Alzheimer Disease, cerebrospinal fluid, diagnosis, Cross-Sectional Studies, Dementia, cerebrospinal fluid, diagnosis, Dementia, Vascular, cerebrospinal fluid, diagnosis, Diagnosis, Differential, Enzyme-Linked Immunosorbent Assay, Epitopes, cerebrospinal fluid, Female, Humans, Lewy Body Disease, cerebrospinal fluid, diagnosis, Male, Middle Aged, Phosphoric Acid Esters, cerebrospinal fluid, Phosphorylation, Predictive Value of Tests, Reference Values, tau Proteins, cerebrospinal fluid
Ämneskategorier Psykiatri

Sammanfattning

BACKGROUND: Abnormal hyperphosphorylation of the microtubule-associated protein tau and its incorporation into neurofibrillary tangles are major hallmarks of the pathogenesis of Alzheimer disease (AD). Different tau phosphoepitopes can be sensitively detected in cerebrospinal fluid (CSF). OBJECTIVE: To compare the diagnostic accuracy of CSF concentrations of tau proteins phosphorylated at 3 pathophysiologically important epitopes (p-tau) to discriminate among patients with AD, nondemented control subjects, and patients with other dementias. DESIGN AND SETTING: Cross-sectional, bicenter, memory clinic-based studies. PARTICIPANTS: One hundred sixty-one patients with a clinical diagnosis of AD, frontotemporal dementia, dementia with Lewy bodies, or vascular dementia and 45 nondemented controls (N = 206). MAIN OUTCOME MEASURES: Levels of tau protein phosphorylated at threonine 231 (p-tau231), threonine 181 (p-tau181), and serine 199 (p-tau199). The CSF p-tau protein levels were measured using 3 different enzyme-linked immunosorbent assays. RESULTS: The mean CSF levels of the studied p-tau proteins were significantly elevated in patients with AD compared with the other groups. Applied as single markers, p-tau231and p-tau181 reached specificity levels greater than 75% between AD and the combined non-AD group when sensitivity was set at 85% or greater. Statistical differences between the assay performances are presented. Particularly, discrimination between AD and dementia with Lewy bodies was maximized using p-tau181at a sensitivity of 94% and a specificity of 64%, and p-tau231 maximized group separation between AD and frontotemporal dementia with a sensitivity of 88% and a specificity of 92%. Combinations of the 3 markers did not add discriminative power compared with the application as single markers. CONCLUSIONS: The p-tau proteins in CSF come closest to fulfilling the criteria of a biological marker of AD. There is a tendency for p-tau proteins to perform differently in the discrimination of primary dementia disorders from AD.

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