Model System:

TBI

Reference Type:

Journal

Accession No.:

J77947

Journal:


Neurorehabilitation and Neural Repair

Year, Volume, Issue, Page(s):

, 30, 10, 920-930

Publication Website:

Abstract:

Study assessed associations of functional polymorphisms in the ankyrin repeat and kinase domain (ANKK1; Taq1a) and catechol-O-methyltransferase (COMT; Val158Met) genes with behavioral dysfunction following traumatic brain injury (TBI). Ninety survivors of severe TBI recruited from a level 1 trauma center were evaluated. The Frontal Systems Behavior Scale, a self- or family report questionnaire evaluating behavior associated with frontal lobe dysfunction, was completed 6 and 12 months postinjury. Depression was measured concurrently with the Patient Health Questionnaire-9. Study participants were genotyped for Val158Met and Taq1a polymorphisms. No statistically significant behavioral differences were observed by Taq1a or Val158Met genotype alone. At 12 months, among those with depression, Met homozygotes (Val158Met) self-reported worse behavior than Val carriers, and A2 homozygotes (Taq1a) self-reported worse behavior than A1 carriers in bivariable analysis. Multivariable models suggest an interaction between depression and genetic variation with behavior at 12 months post-TBI, and descriptive analysis suggests that carriage of both risk alleles may contribute to worse behavioral performance than carriage of either risk allele alone. Findings demonstrate that in the context of depression, Val158Met and Taq1a polymorphisms are individually associated with behavioral dysfunction 12 months following severe TBI, with preliminary evidence suggesting cumulative, or perhaps epistatic, effects of COMT and ANKK1 on behavioral dysfunction.

Author(s):


Myrga, John M., Juengst, Shannon B., Failla, Michelle D., Conley, Yvette P., Arenth, Patricia M., Grace, Anthony A., Wagner, Amy K.

Participating Centers: