To determine the distribution of amyloid precursor protein (APP), monoclonal antibodies against APP45–62 (APP 1-28-9) and β1-17 (4A18 and 4A61) were produced. In the sections of Alzheimer’s disease (AD) brain, APP 1-28-9 was reactive with neurites around senile plaques and a few neurons but not with amyloid cores. This antibody also immunostained the axons in the ischemic lesions of brain tissues from cases with cerebral infarct. 4A18 and 4A61 were reactive with amyloid plaques but not with neurites and neurons. The latter two antibodies also immunostained axons in ischemic lesions. These findings suggest that APP, transported by the fast axonal flows, accumulated in the injured axons in the central nervous system. The β immunoreactivity appearing in those axons may provide a clue to the mechanism of amyloidogenesis.

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