Object: Although plaques composed of amyloid beta (AD) have been found shortly after traumatic brain injury (TBI) in humans, the source for this Abeta has not been identified. In the present study, the authors explored the potential relationship between Abeta accumulation in damaged axons and associated Abeta plaque formation.
Methods: The authors performed an immunohistochemical analysis of paraffin-embedded sections of brain from 12 patients who died after TBI and from two control patients by using antibodies selective for Abeta peptides, amyloid precursor protein (APP), and neurofilament (NF) proteins. In nine brain-injured patients, extensive colocalizations of Abeta, APP, and NF protein were found in swollen axons. Many of these immunoreactive axonal profiles were present close to Abeta plaques or were surrounded by Abeta staining, which spread out into the tissue. Immunoreactive profiles were not found in the brains of the control patients.
Conclusions: The results of this study indicate that damaged axons can serve as a large reservoir of Abeta, which may contribute to Abeta plaque formation after TBI in humans.