Circulating beta amyloid protein is elevated in patients with acute ischemic stroke

P. H. Lee, O. Y. Bang, E. M. Hwang, J. S. Lee, U. S. Joo, I. Mook-Jung, K. Huh

Research output: Contribution to journalArticlepeer-review

51 Citations (Scopus)

Abstract

Recent clinical and experimental studies suggest that ischemic strokes may play an important role in the pathogenesis of Alzheimer's disease (AD). Beta amyloid (Aβ), a major component of senile plaque in AD, is known to be derived from ischemic brain or activated platelets. We prospectively enrolled 62 patients with acute ischemic stroke and 27 age-matched controls. The serum Aβ and P-selectin levels were determined using the Sandwich-ELISA. We divided ischemic strokes into subgroups according to the clinical syndrome, pathogenesis, and infarct size, and compared the Aβ level between each subgroup. The Aβ1-40 level was markedly elevated in ischemic stroke patients, as compared to controls (140.2 ± 54.0 vs 88.44 ± 34.96 pg/ml, p<0.001). Cardioembolic and larger artery atherosclerotic infarcts had higher Aβ1-40 level than small vessel disease (p = 0.001). Both infarct size and the initial NIHSS score had significantly positive correlations with the serum level of Aβ1-40 (r = 0.539, p<0.001 and r = 0.425, p = 0.001, respectively). However, the P-selectin level was not significantly correlated with serum Aβ1-40. Our data suggest that elevated circulating Aβ1-40 in ischemic stroke patients may be derived from brain as a consequence of ischemic insults.

Original languageEnglish
Pages (from-to)1371-1379
Number of pages9
JournalJournal of Neural Transmission
Volume112
Issue number10
DOIs
Publication statusPublished - 2005 Oct

All Science Journal Classification (ASJC) codes

  • Neurology
  • Clinical Neurology
  • Psychiatry and Mental health
  • Biological Psychiatry

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