Accumulation of β-amyloid precursor protein and ubiquitin in axons after spinal cord trauma in humans: immunohistochemical observations on autopsy material

Abstract

We evaluated by immunohistochemistry the presence of β-amyloid precursor protein (ßAPP) and ubiquitin-like material which may accumulate in axons of the human spinal cord subjected to injury. Autopsy material was obtained from nine cases with different types of trauma: breech delivery with neonatal spinal injury, compression of the cord induced by fractures of the vertebral column, haematomas or intradural meningioma. The post-trauma period ranged from 10 days to several years. The spinal cord of six control cases without evidence of injury presented βAPP immunoreactivity in nerve cell bodies and in a few axonal profiles but not in dendrites. Seven of the nine cases with spinal cord trauma showed an accumulation of βAPP-immunoreactive material in axons of the longitudinal tracts at the site of the injury. Five cases presented similar axonal immunoreactivity in the grey matter of the cord. Ubiquitin-like immunoreactivity was present in expanded axons in cases with spinal cord injury. Cases with spinal cord trauma thus present βAPP-immunoreactive axons particularly of the longitudinal tracts in the same way as in trauma to rat spinal cord and in various brain injuries. The aggregation of βAPP-immunoreactive material indicates disturbed axonal transport of βAPP. Accumulation of ubiquitin-like immunoreactive material in expanded axons at the site of trauma may be one prerequisite for degradation of abnormal proteins by the ubiquitin-mediated proteolytic pathway.