Almost two million Americans each year suffer from a traumatic brain injury (TBI). TBI’s occur as a result of physical trauma to the brain. The most common symptoms include headaches, memory loss, depression, and/or personality changes. Upon violent impact to the head, a chemical called glutamate accumulates in the brain. High concentrations of glutamate are lethal to brain cells even though the chemical is responsible for learning and memory under normal conditions. Recently, scientists at Rutgers University asked the question: “can we slow the progress of TBIs by targeting glutamate?”
The study was led by Dr. Bonnie Firestein in the Department of Cell Biology and Neuroscience. The approach is clever and transformative, as most previous efforts to tackle TBI mainly focus on alleviating symptoms instead of preventing progression of the injury itself. The researchers found that combining lithium and rapamycin together, nerve cells stop sending glutamate signals to other cells. This prevents cells for dying off. Lithium is already used to treat depression and bipolar disorder, while rapamycin is typically used against cancer. Most of the work was done in pitri dishes with cultured nerve cells and animal-based trials are currently underway. This may be a very important breakthrough that might especially benefit children. Young patients with concussions may benefit greatly from such a medication by preventing long term effects of cell death in the developing brain.
Przemyslaw Swiatkowski, Ina Nikolaeva, Gaurav Kumar, Avery Zucco, Barbara F. Akum, Mihir V. Patel, Gabriella D’Arcangelo, Bonnie L. Firestein. Role of Akt-independent mTORC1 and GSK3β signaling in sublethal NMDA-induced injury and the recovery of neuronal electrophysiology and survival. Scientific Reports, 2017; 7 (1) DOI: 10.1038/s41598-017-01826-ws
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