Traumatic brain injury, or TBI, represents the primary cause of death and disability in children and young adults. Occurring approximately three times a minute, it affects nearly 2 million people a year in the United States alone. According to the Centers for Disease Control and Prevention, every year TBI leads to more than 2,600 deaths, 37,000 hospitalizations, and 435,000 emergency department visits for children up to age 14.

TBI can occur in a variety of events ranging in severity from an automobile accident to a seemingly innocuous bump on the head that can occur during a child’s normal play. However, even injuries considered mild and associated with limited cognitive effects — like a temporary change in mental status — can set into a motion a cascade of events inside the brain that can lead to long-lasting problems.

Akiva Cohen, PhD, Division of Neurology, is investigating changes in the limbic system of the brain that lead to TBI-induced cognitive impairments. The center of this investigation involves changes in the levels of branched-chain amino acids after TBI.

Using lateral fluid percussion injury coupled with behavioral testing and other laboratory techniques, Dr. Cohen and his colleagues noticed a significant decrease in the levels of these critical branched-chain amino acids in the hippocampus, a part of the brain often injured in TBI that plays a role in higher cognitive functioning such as emotion, learning, and memory. These amino acids are essential for the synthesis of both excitatory (glutamate) and inhibitory (GABA) neurotransmitters. Normal hippocampal function is dependent on the balance between the excitatory and inhibitory systems.

Refurbishing the optimum levels of these amino acids therefore becomes key to minimizing the cognitive effects of mild to moderate TBI by restoring hippocampal function.

Their innovative research has lead to the development of a potential approach to actively and quickly restore the necessary balance between excitatory and inhibitory neurotransmission to the hippocampus before long-term effects can take hold.

“Re-establishing the normal concentration of branched-chain amino acids after injury may lead to the restoration of the balance between excitatory and inhibitory neurotransmission necessary for normal hippocampal function, leading to cognitive improvement after TBI,” says Dr. Cohen.

Dr. Cohen and his colleagues believe that the dietary consumption of these critical branched-chain amino acids, mixed with water and delivered over a period of several days, may bring about this balance and restore the levels of branched-chain amino acids to normal after a mild-to-moderate TBI.

“It is our hope that after further investigation we may have a relatively easy, rapid, and cost-effective way to prevent any devastating, long-term cognitive dysfunction caused by traumatic brain injury,” says Dr. Cohen.