We evaluated by immunohistochemistry the changes of beta-amyloid precursor protein (beta APP) and beta-amyloid peptide (beta A) in the spinal cord of rats with compression injury at Th8-9 of mild, moderate, and severe degrees. The spinal cord of normal rats and animals with laminectomy revealed immunoreactivity to beta APP in nerve cell bodies, the initial part of a few axons of the gray matter, and in scattered glial cells. At 4 h after compression, beta APP-immunoreactivity occurred in a few swollen axons of the longitudinal tracts; such beta APP-immunoreactive axons remained throughout the experimental period of 9 days. The number of immunoreactive axons and the intensity of their immunoreactivity were increased in rats with moderate and severe compression. The caudal Th10 segment exhibited more pronounced accumulation of beta APP immunoreactivity than the cranial Th segment. There was no evidence of beta A accumulation after compression injury. In conclusion, there is a rapidly occurring, long-lasting accumulation of immunoreactive beta-amyloid precursor protein after compression injury of rat spinal cord. This accumulation is related to the degree of impact to the cord.