Alterations of β A4 amyloid protein precursor (APP) were investigated immunohistochemically in the gerbil brain after transient global ischemia and subsequent reperfusion. Marked accumulation of this protein peaking at 24 h occurred in the neurons of the CA3 and paramedian region of the hippocampus as well as layers III, V and VI of the cerebral cortex. On the contrary, the accumulation was not observed in the neurons of the CA1 region. These results indicate that distribution of APP is altered depending on tissue viabilities after cerebral ischemia.
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