Research Reports - Variants of SLC6A4 in depression risk following severe TBI

Brain Inj. 2013 Jun;27(6):696-706

Failla MD, Burkhardt JN, Miller MA, Scanlon JM, Conley YP, Ferrell RE, Wagner AK

BACKGROUND: Post-traumatic depression (PTD) may be a result of several factors
like secondary injury chemical cascades as well as psycho-social factors
following traumatic brain injury (TBI). While the role of serotonin in the
pathology and treatment of idiopathic major depression may be somewhat
controversial, it is unclear what role serotonin may play in PTD following a TBI.
Objective: To assess serotonergic function and genetic risk for PTD development
over 1 year following TBI.
RESEARCH DESIGN: Examination of variation in the serotonin transporter gene
[SLC6A4 (5-HTTLPR, rs25331, and a variable number of tandem repeats variant in
Intron 2)] in 109 subjects with moderate-severe injury. Depression was assessed
using the Patient Health Questionnaire (PHQ-9) at 6 and/or 12 months post-injury.
MAIN OUTCOMES AND RESULTS: At 6 months post-injury, subjects with a history of
pre-morbid mood disorders and 5-HTTLPR L-homozygotes were at greater risk for
PTD. Contrary to major depression, subjects without pre-morbid mood disorders
(n = 80) and S-carriers were 2.803-times less likely to be depressed compared to
L-homozygotes. At 12 months post-injury, LG-carriers were also less likely to
experience PTD. Temporal analysis also showed 5-HTTLPR associations in PTD
development across recovery.
CONCLUSIONS: This study suggests a unique injury- and temporally-specific
interaction between TBI and genetic risk for depression.

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