| Autor: |
Johnson VE; Penn Center for Brain Injury and Repair, The University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA., Stewart W, Graham DI, Stewart JE, Praestgaard AH, Smith DH |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of neurotrauma [J Neurotrauma] 2009 Aug; Vol. 26 (8), pp. 1197-202. |
| DOI: |
10.1089/neu.2008-0843 |
| Abstrakt: |
Traumatic brain injury (TBI) induces the rapid formation of Alzheimer's disease (AD)-like amyloid-beta (AB) plaques in about 30% of patients. However, the mechanisms behind this selective plaque formation are unclear. We investigated a potential association between amyloid deposition acutely after TBI and a genetic polymorphism of the AB-degrading enzyme, neprilysin (n = 81). We found that the length of the GT repeats in AB-accumulators was longer than in non-accumulators. Specifically, there was an increased risk of AB plaques for patients with more than 41 total repeats (p < 0.0001; OR: 10.1). In addition, the presence of 22 repeats in at least one allele was independently associated with plaque deposition (p = 0.03; OR: 5.2). In contrast, the presence of 20 GT repeats in one allele was independently associated with a reduced incidence of AB deposition (p = 0.003). These data suggest a genetically linked mechanism that determines which TBI patients will rapidly form AB plaques. Moreover, these findings provide a potential genetic screening test for individuals at high risk of TBI, such as participants in contact sports and military personnel. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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