Apolipoprotein E-genotype dependent hippocampal and cortical responses to traumatic brain injury
Abstract
The different alleles of the apolipoprotein E gene (APOE-gene, ApoE-protein) have been reported to influence recovery after traumatic brain injury (TBI) in both human patients and animal models, with the e4 allele typically conferring poorer prognosis for recovery. How the E4 allele, and consequently the ApoE4 isoform, affects recovery is unknown, but proposed mechanisms include neurogenesis, inflammatory response and amyloid processing or metabolism. Using the controlled cortical impact (CCI) model of brain injury and microarray technology we have characterized the genomic response to injury in the brains of APOE2, APOE3 and APOE4 transgenic mice and identified quantitatively and qualitatively significantly different profiles of gene expression in both the hippocampus and the cortex of the APOE3 mice compared to APOE4. The observed gene regulation predicts functional consequences including effects on inflammatory processes, cell growth and proliferation, and cellular signaling, and may suggest that the poor recovery post-TBI in APOE4 animals and human patients is less likely to result from a specific activation of neurodegenerative mechanisms than a loss of reparative capability.
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Modifying effects of the different apoe protein isoforms on these pathways are biologically plausible and have been evaluated in experimental model systems.
“modifying effects of the different apoe protein isoforms on these pathways are biologically plausible and have been evaluated in experimental model systems (61).”
From Association of ALS with head injury, cigarette smoking and APOE genotypes (2010) · cites this paper as [61]
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- Authors
- Crawford, F., Wood, M., Ferguson, S., Mathura, V., Gupta, P., Humphrey, J., Mouzon, B., Laporte, V., Margenthaler, E., O'Steen, B., Hayes, R., Roses, A., & Mullan, M.
- Venue
- Neuroscience
- Publisher
- Elsevier BV
- Published
- 2009-04
- Volume
- 159
- Issue
- 4
- Pages
- 1349-1362
- ISSN
- 0306-4522
- Cited by
- 49
- References
- 7
- Language
- en
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