Protein accumulation in traumatic brain injury

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 r...

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Bibliographic Details
Published in:Neuromolecular medicine 2003-01, Vol.4 (1-2), p.59-72
Main Authors: Smith, Douglas H, Uryu, Kunihiro, Saatman, Kathryn E, Trojanowski, John Q, McIntosh, Tracy K
Format: Article
Language:English
Subjects:
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Animals
Axons - metabolism
Axons - pathology
Brain Injuries - complications
Brain Injuries - pathology
Brain Injuries - physiopathology
Causality
Disease Models, Animal
Humans
Mortality
Nerve Tissue Proteins - metabolism
Neurodegeneration
Neurodegenerative Diseases - etiology
Neurodegenerative Diseases - pathology
Neurodegenerative Diseases - physiopathology
Neurofilament Proteins - metabolism
Parkinson's disease
Synucleins
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Summary: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; beta-amyloid precursor protein and its proteolytic products, amyloid-beta (Abeta) 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.
ISSN:1535-1084
1559-1174
1535-1084
DOI:10.1385/nmm:4:1-2:59