Association of increased cortical soluble abeta42 levels with diffuse plaques after severe brain injury in humans.

@article{DeKosky2007AssociationOI,
  title={Association of increased cortical soluble abeta42 levels with diffuse plaques after severe brain injury in humans.},
  author={Steven DeKosky and Eric E. Abrahamson and John R Ciallella and William R. Paljug and Stephen R. Wisniewski and Robert S B Clark and Milos D. Ikonomovic},
  journal={Archives of neurology},
  year={2007},
  volume={64 4},
  pages={541-4}
}
BACKGROUND Traumatic brain injury (TBI) is an environmental risk factor for developing Alzheimer disease. This may be due, in part, to changes associated with beta-amyloid (Abeta) plaque formation, which can occur within hours after injury, regardless of the patient's age. In addition to being precursors of toxic fibrils that deposit into plaques, soluble… CONTINUE READING