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Evaluation of CSF biomarkers for axonal and neuronal degeneration, gliosis, and β-amyloid metabolism in Alzheimer's disease
  1. N ANDREASEN
  1. Department of Rehabilitation, Piteå River Valley Hospital, PO Box 715, SE-941 28 Piteå, Sweden
  2. Astra-Zeneca, Mölndal, Sweden
  3. Innogenetics, Ghent, Belgium
  4. Department of Clinical Neuroscience, Section of Experimental Neuroscience, University of Göteborg, Sahlgren's University Hospital, Mölndal, Sweden
  5. Department of Clinical Neuroscience, Section of Neurology, University of Göteborg, Sahlgren's University Hospital, Göteborg, Sweden
  6. The Medical Research Council, Sweden
  1. Dr N Andreasen niels.andreasen{at}nll.se
  1. J GOTTFRIES
  1. Department of Rehabilitation, Piteå River Valley Hospital, PO Box 715, SE-941 28 Piteå, Sweden
  2. Astra-Zeneca, Mölndal, Sweden
  3. Innogenetics, Ghent, Belgium
  4. Department of Clinical Neuroscience, Section of Experimental Neuroscience, University of Göteborg, Sahlgren's University Hospital, Mölndal, Sweden
  5. Department of Clinical Neuroscience, Section of Neurology, University of Göteborg, Sahlgren's University Hospital, Göteborg, Sweden
  6. The Medical Research Council, Sweden
  1. Dr N Andreasen niels.andreasen{at}nll.se
  1. E VANMECHELEN,
  2. H VANDERSTICHELE
  1. Department of Rehabilitation, Piteå River Valley Hospital, PO Box 715, SE-941 28 Piteå, Sweden
  2. Astra-Zeneca, Mölndal, Sweden
  3. Innogenetics, Ghent, Belgium
  4. Department of Clinical Neuroscience, Section of Experimental Neuroscience, University of Göteborg, Sahlgren's University Hospital, Mölndal, Sweden
  5. Department of Clinical Neuroscience, Section of Neurology, University of Göteborg, Sahlgren's University Hospital, Göteborg, Sweden
  6. The Medical Research Council, Sweden
  1. Dr N Andreasen niels.andreasen{at}nll.se
  1. P DAVIDSSON,
  2. K BLENNOW
  1. Department of Rehabilitation, Piteå River Valley Hospital, PO Box 715, SE-941 28 Piteå, Sweden
  2. Astra-Zeneca, Mölndal, Sweden
  3. Innogenetics, Ghent, Belgium
  4. Department of Clinical Neuroscience, Section of Experimental Neuroscience, University of Göteborg, Sahlgren's University Hospital, Mölndal, Sweden
  5. Department of Clinical Neuroscience, Section of Neurology, University of Göteborg, Sahlgren's University Hospital, Göteborg, Sweden
  6. The Medical Research Council, Sweden
  1. Dr N Andreasen niels.andreasen{at}nll.se
  1. L ROSENGREN
  1. Department of Rehabilitation, Piteå River Valley Hospital, PO Box 715, SE-941 28 Piteå, Sweden
  2. Astra-Zeneca, Mölndal, Sweden
  3. Innogenetics, Ghent, Belgium
  4. Department of Clinical Neuroscience, Section of Experimental Neuroscience, University of Göteborg, Sahlgren's University Hospital, Mölndal, Sweden
  5. Department of Clinical Neuroscience, Section of Neurology, University of Göteborg, Sahlgren's University Hospital, Göteborg, Sweden
  6. The Medical Research Council, Sweden
  1. Dr N Andreasen niels.andreasen{at}nll.se
  1. K BLENNOW
  1. Department of Rehabilitation, Piteå River Valley Hospital, PO Box 715, SE-941 28 Piteå, Sweden
  2. Astra-Zeneca, Mölndal, Sweden
  3. Innogenetics, Ghent, Belgium
  4. Department of Clinical Neuroscience, Section of Experimental Neuroscience, University of Göteborg, Sahlgren's University Hospital, Mölndal, Sweden
  5. Department of Clinical Neuroscience, Section of Neurology, University of Göteborg, Sahlgren's University Hospital, Göteborg, Sweden
  6. The Medical Research Council, Sweden
  1. Dr N Andreasen niels.andreasen{at}nll.se

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Although the accuracy rate of the clinical diagnosis of Alzheimer's disease is around 75%–90%, it is probably considerably lower early in the disease course, when symptoms are vague. Therefore, in view of potential future disease modifying compounds there is a great need for reliable diagnostic biochemical markers for Alzheimer's disease in CSF.

Such markers should reflect the central pathogenic processes of the disease—that is, the disturbance in the metabolism of β-amyloid (Aβ) with subsequent Aβ deposition in senile plaques, the hyperphosphorylation of tau protein with subsequent formation of neurofibrillary tangles, neuronal degeneration, and gliosis.

Two promising biomarkers are tau protein (reflecting neuronal and axonal degeneration) and Aβ42 (reflecting disturbances in Aβ metabolism and possibly Aβ deposition in senile plaques). The ability of the combination of CSF tau and CSF Aβ42 to differentiate Alzheimer's disease from normal aging and depression is high, about 85%, also early in the course of the disease.1 Similarly, most degenerative neurological disorders have normal concentrations. However, the specificity against other dementias is not optimal.1 Thus, there is a need for additional CSF biomarkers for Alzheimer's disease, to further increase the diagnostic accuracy.

We therefore examined whether the addition of other CSF biomarkers (two neuronal and two glial proteins) …

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