Excess glutamate causes persistent opening of glutamate-gated ion channels, hyperexcitation and loss of homeostasis. This effect is called glutamate excitotoxicity.  The delicate balance between glutamate (excitatory) and GABA (inhibitory) neurotransmission becomes skewed.  Overexcitation by glutamate obliges a neuron to consume significantly more energy to maintain membrane voltage potentials. Energy depletion is countered by increased mitochondrial

Traumatic Brain Injury (TBI)

TBI is an acute insult, often caused by blunt force impact to the head, causing waves that stretch and twist neurons and their axons throughout the brain. These effects can lead to neuronal damage by direct physical disruption of cell membranes. Among the many compounds released into the extracellular space when neuronal integrity is breached, glutamate is particularly pathogenic.

“We have spent 11 years following our data, and it has led us to this discovery. We ask questions based on the data and follow the evidence wherever it leads us.”

   - Sara, CEO and Co-founder

activity and its consequence, elevated levels of reactive oxygen species (ROS).  Elevated intracellular calcium adds additional strain on mitochondria and the endoplasmic reticulum, which sacrificially sequester calcium in favor of the cytoplasm. Mitochondrial failure from excessive ROS and calcium levels leads to apoptosis of the neuron, releasing more glutamate into the extracellular space and perpetuation of the damage.  This cataclysm of runaway neurotransmission has been termed a glutamate storm. Propagation of damage from the initial insult may continue for years, turning acute injury into progressive neurodegeneration.

Depiction of neuronal activity inside brain. When injured by a degenerative disease or blunt trauma, this firing goes out of control. Mainly triggered by a glutamate storm causing further damage to neighboring cells, leading to progression of the disease.

At this stage, we have finished screening and have a number of candidates. We will be initiating efficacy and associated studies in three disease models: traumatic brain injury (TBI), stroke, and amyotrophic lateral sclerosis (ALS). 

Amyotrophic lateral sclerosis (ALS)

Unlike TBI and stroke, amyotrophic lateral sclerosis (ALS) is a chronic neurodegenerative disease. Although chronic, the reasons for neuronal death are the same as in the case of acute neurodegeneration. In ALS, once symptoms are diagnosed, motor-neurons are already degenerating. Aggregates of proteins such as TDP-43 and SOD1 in the neuronal cell lead to progression of the disease.

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In cases of stroke, blood vessel occlusion causes areas of the brain to become hypoxic.  In response, affected cells downregulate antioxidant systems. If the occlusion is removed, oxygen-rich blood returns to the area, a process called reperfusion. Reperfusion of neurons with poor antioxidant reserves causes oxidative stress.  Neurons that die upon reperfusion release their contents into the extracellular space, including glutamate, leading to excitotoxicity and additional neuronal death.