NeuroMolecular Medicine

, Volume 4, Issue 1, pp 59–72

Protein accumulation in traumatic brain injury

Authors

    • Department of NeurosurgeryUniversity of Pennsylvania
  • Kunihiro Uryu
    • Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory MedicineUniversity of Pennsylvania
  • Kathryn E. Saatman
    • Department of NeurosurgeryUniversity of Pennsylvania
  • John Q. Trojanowski
    • Center for Neurodegenerative Disease Research, Department of Pathology and Laboratory MedicineUniversity of Pennsylvania
    • Institute on AgingUniversity of Pennsylvania
  • Tracy K. McIntosh
    • Department of NeurosurgeryUniversity of Pennsylvania
    • Veterans Administration Medical Center
Article

DOI: 10.1385/NMM:4:1-2:59

Cite this article as:
Smith, D.H., Uryu, K., Saatman, K.E. et al. Neuromol Med (2003) 4: 59. doi:10.1385/NMM:4:1-2:59

Abstract

Traumatic brain injury (TBI) is one of the most devastating diseases in our society, accounting for a high percentage of mortality and disability. A major consequence of TBI is the rapid and long-term accumulation of proteins. This process largely reflects the interruption of axonal transport as a result of extensive axonal injury. Although many proteins are found accumulating after TBI, three have received particular attention; β-amyloid precursor protein and its proteolytic products, amyloid-β (Aβ) peptides, neurofilament proteins, and synuclein proteins. Massive coaccumulations of all of these proteins are found in damaged axons throughout the white matter after TBI. Additionally, these proteins form aggregates in other neuronal compartments and in brain parenchyma after brain trauma. Interestingly, TBI is also an epigenetic risk factor for developing neurodegenerative disorders, such as Alzheimer’s disease and Parkinson’s disease. Here, the similarities and differences of these accumulations with pathologies of neurodegenerative diseases will be explored. In addition, the potential deleterious roles of protein accumulations on functional outcome and progressive neurodegeneration following TBI will be examined.

Index Entries

Traumatic brain injuryTBI, brain traumadiffuse axonal injuryDAI, amyloid precursor proteinAPP, amyloid-βneurofilament proteinssynuclein proteinsaccumulation

Copyright information

© Humana Press Inc 2003