Traumatic brain jury (TBI) and associated co-morbidities are important contributors of disability among military personnel. Therefore, it is an urgent need to find an effective, a safe and an economical solution for this. Axonal injury is an important contributor to the behavioral deficits observed following TBI. It is believed that axonal injury during TBI is potentiated by neuroinflammation and demyelination and/or failure to remyelination. Cinnamon is a commonly used flavoring material and its metabolite sodium benzoate (NaB) is a widely-used food preservative and a FDA-approved drug for the treatment of urea cycle disorders and non-ketotic hyperglycinemia in children. Here, we will examine an exciting hypothesis that cinnamon metabolite NaB binds to the ligand-binding domain of peroxisome proliferator-activated receptor beta (PPAR?) (Specific aim I) to induce anti-inflammation in microglia and promote maturation of OPCs (Specific aim II), resulting in neuroprotection in a mouse model of TBI (Specific aim III). A positive outcome of this cutting-edge merit proposal will delineate NaB as a new nontoxic ligand of PPAR? and enhance the possibility of attenuating microglial activation, promoting remyelination and treating TBI patients with cinnamon and its metabolite NaB as primary or adjunct therapy.
Suppressing neuroinflammation and promoting remyelination is an important area of research. Here, we will test a novel idea that cinnamon metabolite sodium benzoate binds to peroxisome proliferator-activated receptor ? to stimulate anti-inflammation and promote remyelination, leading to neuroprotection in an animal model of traumatic brain injury. This study will enhance the possibility of attenuating neuroinflammation, stimulating remyelination and treating patients with traumatic brain injury with cinnamon and its metabolite sodium benzoate as primary or adjunct therapy. 1
