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Our research goal
To develop unique therapeutic approaches to inhibit glutamate excitotoxicity in neurotrauma, degenerative and psychiatric diseases

Research questions

What damage causes excess extracellular glutamate in pathological conditions of the central nervous system and how can we prevent the damage through our new anti-glutamate therapy?

Unmeet need: Excitotoxicity

Glutamate is the major excitatory neurotransmitter in the brain. Forty years of data have consistently shown that high levels of extracellular glutamate in the brain can damage and kill neurons. Recognition of this phenomenon (“excitotoxicity”) spawned intensive research in the fields of neurotrauma, neurodegenerative and maligning diseases which discovered that a high level of extracellular glutamate in the brain leads to an overload of intracellular calcium resulting in the death of neurons.






Our solution:

Blood-glutamate scavenging as an emergency treatment that reduces excitotoxicity

We have developed a radically different strategy to reduce Glu excitotoxicity. We will enhance a natural blood-resident enzymatic system that reduces the blood levels of glutamate to produce a brain-to-blood gradient that will then reduce the CNS levels of the excess Glu. 

Blood-glutamate scavenging emergency treatment for spinal cord injury

Excitotoxicity due to neuronal damage and glutamate release is one of the first events that leads to the progression of neuronal degeneration and functional impairment. This study is based on a paradigm shift in the therapeutic approach for treating spinal cord injury (SCI). We are developing the first emergency treatment for SCI blood-glutamate scavengers (BGS). 

In SCI mice model BGS treatment decreased the CSF glutamate level up to 50%, reduced axonal wallerian degeneration, and increased axonal survival and GAP-43 expression in neuronal cells. In addition, the motor function significantly improved in the treated group post-SCI.

Conclusions: As shown by biochemical, immunohistochemical, and functional analysis, BGSs exhibit a substantial neuroprotective effect by reducing excitotoxicity and secondary damage after SCI.

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