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Brain Advance Access published online on September 29, 2006
Brain, doi:10.1093/brain/awl269
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received August 7, 2006
Revised August 30, 2006
Accepted August 31, 2006

Article

CSF phosphorylated tau protein correlates with neocortical neurofibrillary pathology in Alzheimer's disease

Katharina Buerger 1 * *, Michael Ewers 1 *, Tuula Pirttilä 2, Raymond Zinkowski 3, Irina Alafuzoff 4, Stefan J. Teipel 1, John DeBernardis 3, Daniel Kerkman 3, Cheryl McCulloch 3, Hilkka Soininen 2, and Harald Hampel 1

1 Dementia Research Section and Memory Clinic, Alzheimer Memorial Center, Department of Psychiatry, Ludwig-Maximilian University, Munich, Germany
2 Department of Neuroscience and Neurology, Kuopio University Hospital, University of Kuopio, Kuopio, Finland
3 Applied NeuroSolutions Inc., Vernon Hills, IL, USA
4 Department of Pathology, Kuopio University Hospital, University of Kuopio, Kuopio, Finland

* To whom correspondence should be addressed.
Katharina Buerger, E-mail: katharina.buerger{at}med.uni-muenchen.de


  Abstract

Hyperphosphorylated tau protein (P-tau) in CSF is a core biomarker candidate of Alzheimer's disease. Hyperphosphorylation of tau is thought to lead to neurofibrillary changes, a neuropathological hallmark of this type of dementia. Currently, the question is unresolved whether CSF levels of P-tau reflect neurofibrillary changes within the brain of a patient with the illness. Twenty-six patients were included with intra-vitam CSF as well as post-mortem neuropathological data. In the CSF, P-tau phosphorylated at threonine 231 (P-tau231P) was analysed. Post-mortem, scores of neurofibrillary tangles (NFT) and neuritic plaques (NP) were assessed in frontal, temporal, parietal and hippocampal cortical areas. In the same cortical regions, load of hyperphosphorylated tau protein (HP-tau load) was determined. Concentrations of P-tau231P were measured in frontal cortex homogenates. We found significant correlations between CSF P-tau231P concentrations and scores of NFTs and HP-tau load in all neocortical regions studied. The score of NPs was correlated with CSF P-tau231P only within the frontal cortex. There was a correlation between P-tau231P in CSF and brain homogenates. These findings indicate that CSF P-tau231P may serve as an in vivo surrogate biomarker of neurofibrillary pathology in Alzheimer's disease.

Keywords: hyperphosphorylated tau protein; CSF; neuropathology; Alzheimer's disease.
*These authors contributed equally to this work.
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