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Brain-Derived Neurotrophic Factor Val66Met Polymorphism and Internalizing Behaviors after Early Mild Traumatic Brain
Charlotte Gagner1,2, Carola Tuerk1, Louis De Beaumont3,4
1Department of Psychology, University of Montreal, Montréal, Québec, Canada.
Insights
The Val66Met gene polymorphism may protect young children from internalizing behaviors after mild traumatic brain injury (mTBI) for up to six months. However, all children with mTBI showed increased internalizing symptoms at 18 months.
Area of Science:
- Neuroscience
- Genetics
- Pediatric Psychology
Background:
- Pediatric traumatic brain injury (TBI) can cause lasting emotional and behavioral issues.
- Individual variability in TBI outcomes suggests genetic factors influence neuroplasticity and recovery.
- The brain-derived neurotrophic factor (BDNF) Val66Met gene polymorphism is implicated in neuroplasticity.
Purpose of the Study:
- To investigate the impact of the BDNF Val66Met polymorphism on behavioral symptoms in early childhood mild TBI (mTBI).
- To determine if genetic variations modulate neuroplasticity and influence TBI outcomes.
Main Methods:
- A prospective, longitudinal cohort study included 145 children (18-60 months) in three groups: mTBI, orthopedic injury, and typically developing.
- Saliva samples were used to genotype the BDNF Val66Met polymorphism.
- The Child Behavior Checklist assessed behavioral symptoms at 6 and 18 months post-injury.
Main Results:
- At 6 months post-injury, mTBI children without the Val66Met polymorphism showed more internalizing symptoms (anxiety, depression) than carriers.
- Val66Met carriers in the mTBI group exhibited similar internalizing symptoms to control groups at 6 months.
- By 18 months post-injury, all mTBI children displayed increased internalizing symptoms, irrespective of genotype.
Conclusions:
- The BDNF Val66Met polymorphism appears to offer a protective effect against internalizing behaviors in the early aftermath of pediatric mTBI.
- This genetic factor's influence on behavior diminishes over time, as all mTBI children show elevated symptoms by 18 months.
Abstract:
Pediatric traumatic brain injury (TBI) can lead to adverse emotional, social, and behavioral consequences. However, outcome is difficult to predict due to significant individual variability, likely reflecting a complex interaction between injury- and child-related variables. Among these variables are genetically determined individual differences, which can modulate TBI outcome through their influence on neuroplasticity mechanisms. In this study, we examined the effect of Val66Met, a common polymorphism of the brain-derived neurotrophic factor gene known to be involved in neuroplasticity mechanisms, on behavioral symptoms of mild TBI (mTBI) sustained in early childhood. This work is part of a prospective, longitudinal cohort study of early TBI. The current sample consisted of 145 children between ages 18 and 60 months assigned to one of three participant groups: mild TBI, orthopedic injury, or typically developing children. Participants provided a saliva sample to detect the presence of the Val66Met polymorphism, and the Child Behavior Checklist was used to document the presence of behavioral symptoms at 6- and 18-months post-injury. Contrary to our initial hypothesis, at 6 months post-injury, non-carriers of the Val66Met polymorphism in the mTBI group presented significantly more internalizing symptoms (e.g., anxiety/depression and somatic complaints) than Val66Met carriers, who were similar to orthopedically injured and typically developing children. However, at 18 months post-injury, all children with mTBI presented more internalizing symptoms, independent of genotype. The results of the study provide evidence for a protective effect of the Val66Met polymorphism on internalizing behavior symptoms 6 months after early childhood mTBI.
