It has been demonstrated recently that beta-amyloid protein (beta AP), generally associated with the plaques of Alzheimer's disease, can also be found in the brains of survivors of head injury. In this study the distribution of the beta AP precursor protein (beta APP) was examined immunohistochemically to determine if it is colocalized with beta AP in such cases. beta APP immunoreactivity was observed in neuronal perikarya in the neocortex and in dystrophic neurites surrounding beta AP immunoreactive plaques i.e. in a distribution similar to that seen in Alzheimer's disease. In addition, beta APP immunoreactivity was noted within white matter tracts where it marked damaged axons. However, no colocalisation of beta APP with beta AP was observed in any white matter region. These results indicate that processing of beta APP to produce beta AP occurs in the synaptic terminal field of axons and illustrate the utility of beta APP immunoreactivity as a general marker for axonal injury.