The Role of Genetics in TBI Recovery
Horsburgh
et. al.
Mayeux et. al.
Horsburgh, K., Graham, D., B.C.H, Stewart, J., & Nicoll, J. (1999). Influence of Apolipoprotein E Genotype on Neuronal Damage and ApoE Immunoreactivity in Human Hippocampus Following Global Ischemia. Journal of Neuropathology and Experimental Neurology, 58, 227-234.
The purpose of this study was to determine (a) if ApoE is increased in neurons and glia following brain injury in humans, (b) if alterations in neuronal and glial ApoE are ApoE genotype dependent and (c) weather ApoE genotype is associated with worsened neuronal damage following global ischemia. In a broad sense this study was conducted to determine if ApoE causes alterations in neuronal repair mechanisms following an injury. Subjects consisted of 58 patients who died from cardiorespiratory arrest after having survived a previous episode of global ischemia. 44 control patients without clinical or pathological evidence of neurological or psychological impairments or cardiovascular disease were used in the study. ApoE genotyping was performed on embedded blocks of the medial temporal lobe of each of the deceased subjects. Results in individuals with global ischemia showed greater neuronal damage in hippocampal regions and the neo-cortex compared to controls. Following global ischemia in humans, ApoE increased in glia and is markedly increased in neurons. No evidence was found that the apoE influenced the extent of glial apoE, neuronal apoE, or neuronal damage. ApoeE is predominantly localized to ischemic neurons. Possession of ApoE-e4 allele did not influence the degree of glial or neuronal ApoE nor neuronal damage following global ischemia.
Mayeux, R., Ottman, R., Maestre, G., Ngai, C., Tang, X., Ginsberg, H. Chun, M., Tycko, B., & Shelanski, M. (1995). Synergistic effects of traumatic head injury and apolipoprotein-e4 in patients with Alzheimer's disease. Neurology, 45, 555-557.
The purpose of this study was to determine if there is a direct relation between an increased risks of Alzheimer's Disease (AD) and a reaction between ApoE-e4 and injury to the brain. 236 community-dwelling elderly persons participated in the study, 113 of whom met the criteria for AD and the rest were healthy elderly persons. DNA tests conducted to determine the presence or absence of apoE-e4 with a history of brain injury had a ten-fold increase in risk for AD. Subjects carrying ApoE-e4 without a history of TBI had a two-fold increase in risk for Alzheimer's Disease. Subjects with a history of head injury and an absence of the apoE-e4 gene showed no increase risk for AD. This implies that the biological effects of head injury combined with the effects of ApoE-e4 may increase a persons risk for AD. Either one alone has little or no impact on an increased risk for AD.
 |
|