| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Research Abstract |
In the brains of Alsheimer' s disease patients, beta amyloid protein (βAP) is the major component of senile plaque. In ischemic stress, beta amyloid precursor protein (APP) and βAP are reported to be upregulated. Using Male Wister-ST rats, expression and distribution Of APP and βAP were examined immunohistochemically after transient ischemia induced by a 15-min, 30-min and 2-h middle cerebral artery occlusion (MCAO). Astrocyte and microglia were determined immunohistochemically by GFAP, OX42. APP-positive astrocytes were distributed at striatum, cortex and corpus callosum in and around the infarction. APP was expressed in 3, 7 days following the MCAO. In the next year, after reperfusion for 3, 7, 14, 30 and 60 days following 2-h MCAO, brains were removed and immunostaining including APP, βAP and Conco red was performed. The reactive astrocytes with APP were observed in the periphery of infarct from 3 days to 60 days post-occlusion. The immunoreactivity of βAP 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. 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.
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