Authors: P H Lee O Y Bang E M Hwang J S Lee U S Joo I MookJung K Huh
Publish Date: 2005/01/31
Volume: 112, Issue: 10, Pages: 1371-1379
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 agematched controls The serum Aβ and Pselectin levels were determined using the SandwichELISA 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 1402 ± 540 vs 8844 ± 3496 pg/ml p0001 Cardioembolic and larger artery atherosclerotic infarcts had higher Aβ1–40 level than small vessel disease p = 0001 Both infarct size and the initial NIHSS score had significantly positive correlations with the serum level of Aβ1–40 r = 0539 p0001 and r = 0425 p = 0001 respectively However the Pselectin 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
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