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Table of Contents
Vol. 29, No. 6, 2010
Issue release date: July 2010
Dement Geriatr Cogn Disord 2010;29:530–533
(DOI:10.1159/000314679)

CSF-Tau and CSF-Aβ1–42 in Posterior Cortical Atrophy

Baumann T.P. · Duyar H. · Sollberger M. · Kuhle J. · Regeniter A. · Gomez-Mancilla B. · Schmidtke K. · Monsch A.U.
aMemory Clinic – Neuropsychology Center, Departments of Geriatrics, bDepartment of Neurology, and cCSF Laboratory, University Hospital, and dNeurosciences, NS Discovery, Novartis Pharma AG, Basel, Switzerland; eCenter for Geriatric Medicine and Gerontology, University Hospital Freiburg, Freiburg, Germany

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Abstract

Objective: Our purpose was to measure Aβ1–42, T-tau and P-tau181 in the cerebrospinal fluid (CSF) of patients with posterior cortical atrophy (PCA), a presenile dementia likely to represent a variant of Alzheimer’s disease (AD). Methods: CSF samples from 34 subjects including 9 patients with PCA, 11 age-matched patients with AD and 14 age-matched cognitively healthy controls were analyzed using commercially available ELISA kits. Results: The Aβ1–42, T-tau and P-tau181 levels in PCA patients differed significantly (p < 0.02) from those in healthy controls but were indistinguishable from subjects with a clinical diagnosis of AD. Conclusion: High T-tau and P-tau181 and low Aβ1–42 levels in PCA – typically observed in AD – indicate that the underlying pathology of PCA is usually AD. If these findings are replicated in PCA patients with autopsy-confirmed AD neuropathology, PCA patients may be eligible for disease-modifying AD treatments.



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    External Resources

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