Affiliations: [a] Department of Clinical Neuroscience, Unit of Neurochemistry, University of Göteborg, Sahlgren's University Hospital/Mölndal, Sweden | [b] Department of Clinical Neuroscience, Unit of Neurology, University of Göteborg, Sahlgren's University Hospital/Sahlgrenska, Sweden | [c] Department of Clinical Neuroscience, Unit of Radiology, University of Göteborg, Sahlgren's University Hospital/Sahlgrenska, Sweden | [d] Innogenetics NV, Gent, Belgium
Correspondence:
[*]
Corresponding author: C. Hesse, Department of Clinical Neuroscience, Unit of Neurochemistry, University of Göteborg, Sahlgren's University Hospital/Mölndal, S-431 80 Mölndal, Sweden. Tel: +46 31 3432415; Fax: +46 31 3432426; E-mail: [email protected]
Abstract: Potential cerebrospinal fluid (CSF) markers for Alzheimer's disease (AD) include tau protein, the 42 amino-acid form of amyloid ß (amyloid ß(1-42)) and apolipoprotein E (apoE). To study new aspects of these protein markers, we examined consecutive CSF samples from 26 patients with acute ischemic stroke. CSF samples were taken on day 0–1, day 2–3, day 7–9, 3 weeks and 3–5 months after the stroke. CSF-tau showed a marked increase day 2–3, which peaked after 1 week and returned to normal after 3–5 months. CSF-tau also showed correlation (r = 0.95; p < 0.01) with the size of the infarct. In contrast, CSF-amyloid ß(1-42) and CSF-apoE showed no significant changes during the period. The marked increase in CSF-tau levels after acute ischemic stroke indicate that CSF-tau reflect the degree of neuronal damage. The reason for unchanged levels of CSF-amyloid ß(1-42) and CSF-apoE after ischemic stroke remains unclear.
