Expression and distribution of beta amyloid precursor protein and beta amyloid peptide in reactive astrocytes after transient middle cerebral artery occlusion

Background. In the brains of Alzheimer's disease patients, beta amyloid pro tein is the major component of senile plaque. In ischemic stress, beta amyl oid precursor protein (APP) and beta amyloid peptide are reported to be upr egulated. Method. Using Male Wistar-ST rats, expression and distribution of APP and b eta amyloid peptide were examined immunohistochemically after transient isc hemia induced by a 2-h middle cerebral artery occlusion (MCAO). After reper fusion for 3, 7, 14, 30 and 60 days, brains were removed and immunostaining was performed. Findings. The reactive astrocytes with APP were observed in the periphery o f infarct from 3 days to 60 days post-occlusion. The immunoreactivity of be ta amyloid peptide was also localized in the reactive astrocytes in the per ipheral zone of infarct at 7, 14, and 30 days post-occlusion. However, beta amyloid expression was not identified at 3 days or 60 days post MCAO. Tran sient ischemia temporarily induced beta amyloid peptide expression in react ive astrocytes, but this expression peaked at 30 days and disappeared at 60 days. Interpretation. These findings suggested that beta amyloid peptide was deri ved from the processing of APP produced in the same reactive astrocytes and the production of the peptide stopped within 60 days after the ischemic st ress.