Journal
NEUROMOLECULAR MEDICINE
Volume 4, Issue 1-2, Pages 59-72Publisher
HUMANA PRESS INC
DOI: 10.1385/NMM:4:1-2:59
Keywords
traumatic brain injury; TBI, brain trauma; diffuse axonal injury; DAI, amyloid precursor protein; APP; amyloid-beta; A beta; neurofilament proteins; synuclein proteins; accumulation
Categories
Funding
- NIA NIH HHS [AG12527, AG11542] Funding Source: Medline
- NIGMS NIH HHS [R01-GM34790] Funding Source: Medline
- NINDS NIH HHS [R01-NS40978, NS-45131, NS38104, P50-NS08803] Funding Source: Medline
- PHS HHS [AB10124] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS038104, R01NS040978, R01NS045131, P50NS008803] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [P01AG011542, R01AG012527] Funding Source: NIH RePORTER
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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.
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