Background: In the brains of Alzheimer's disease patients, beta amyloid protein is the major component of senile plaque. In ischemic stress, beta amyloid precursor protein (APP) and beta amyloid peptide are reported to be upregulated.
Method: Using Male Wistar-ST rats, expression and distribution of APP and beta amyloid peptide were examined immunohistochemically after transient ischemia induced by a 2-h middle cerebral artery occlusion (MCAO). After reperfusion 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 of infarct from 3 days to 60 days post-occlusion. The immunoreactivity of beta amyloid peptide was also localized in the reactive astrocytes in the peripheral 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. Transient ischemia temporarily induced beta amyloid peptide expression in reactive astrocytes, but this expression peaked at 30 days and disappeared at 60 days.
Interpretation: These findings suggested that beta amyloid peptide was derived from the processing of APP produced in the same reactive astrocytes and the production of the peptide stopped within 60 days after the ischemic stress.