Changes of β-Amyloid Precursor Protein after Compression Trauma to the Spinal Cord: An Experimental Study in the Rat Using Immunohistochemistry

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Abstract
We evaluated by immunohistochemistry the changes of β-amyloid precursor protein (βAPP) and β-amyloid peptide (βA) 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 βAPP 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, βAPP-immunoreactivity occurred in a few swollen axons of the longitudinal tracts; such βAPP-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 βAPP immunoreactivity than the cranial Th segment. There was no evidence of βA accumulation after compression injury. In conclusion, there is a rapidly occurring, long-lasting accumulation of immunoreactive β-amyloid precursor protein after compression injury of rat spinal cord. This accumulation is related to the degree of impact to the cord. Key words: β-amyloid precursor protein, rat, spinal cord, trauma