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| Research article summary (published 5 Feb 2007): |
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Apolipoprotein E and traumatic brain injury in a military population: evidence of a neuropsychological compensatory mechanism?
Full Abstract
OBJECTIVE:
Although research has implicated the apolipoprotein E (APOE) epsilon-4 genotype as having a negative effect on neuropsychological outcomes following traumatic brain injury (TBI), the potentially negative role of the epsilon4 allele on TBI outcomes has recently been challenged. In light of this debate, the present study served to examine the role of APOE genotype on neuropsychological outcomes approximately 1 month following mild to moderate TBI in a military population. Because of the well documented role of the APOE-epsilon4 allele in increasing the risk of Alzheimer's disease, we predicted that persons with the APOE-epsilon4 genotype would display relatively greater deficits in cognition than their non-epsilon4 counterparts.
METHODS:
78 participants were consecutively recruited following a mild to moderate TBI and were divided into two groups based on the presence or absence of an APOE epsilon4 allele. Groups were comparable on demographic characteristics and psychosocial outcomes. Participants were administered a comprehensive neuropsychological battery.
RESULTS:
Analyses revealed comparable performances on most neuropsychological measures and better performances by epsilon4 carriers on select measures of attention, executive functioning and episodic memory encoding. Furthermore, differences remained after accounting for the effects of TBI severity.
CONCLUSIONS:
Evidence from these analyses supports current literature refuting the notion of relatively poorer neuropsychological functioning associated with the APOE-epsilon4 genotype among young adult participants shortly following mild or moderate brain injury. Neuropsychological performance differences by APOE genotype following TBI are discussed in terms of the importance of considering severity of injury, timing of postinjury assessment and possible neurocognitive compensatory mechanisms.
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Author information
Author/s: Han, S Duke (SD); Drake, Angela I (AI); Cessante, Lynne M (LM); Jak, Amy J (AJ); Houston, Wes S (WS); Delis, Dean C (DC); Filoteo, J Vincent (JV); Bondi, Mark W (MW);
Affiliation: Department of Psychology, Loyola University Chicago, Chicago, Illinois, USA.
Journal and publication information
Publication Type: Journal Article; Research Support, U.S. Gov't, Non-P.H.S.
Journal: Journal of neurology, neurosurgery, and psychiatry (J Neurol Neurosurg Psychiatry), published in England. (Language: eng)
Reference: 2007-Oct; vol 78 (issue 10) : pp 1103-8
Dates: Created 2007/09/19; Completed 2007/10/01;
PMID: 17287237, status: MEDLINE (last retrieval date: 12/26/2008)
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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