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Therapeutic Targets for Traumatic Brain Injury

Detailed Technology Description

Georgetown University is seeking a licensing partner interested in thedevelopment of therapeutic treatments for traumatic brain injury (TBI).TBI is the leading cause of mortality and disability among youngindividuals in developed countries. Currently, there is no effectivetreatment for patients following TBI. The initial injury inducesbiochemical and cellular changes that contribute to continuing neuronaldamage and death over time. This continuing damage is known assecondary injury. Post mortem studies have shown that 30% of TBIfatalities have amyloid-beta deposits, which may occur less than 1 daypost injury. Georgetown researchers have shown in a recent NatureMedicine paper that blocking either beta- or gamma-secretase, proteinsresponsible for amyloid-beta production, can dramatically reduce motorand cognitive defects and reduce cell loss after experimental TBI.

*Abstract

*Publications

“Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury.” Nature Medicine. 2009,15 (4), 377-379.

*Stage of Development

Mice were subjected to a controlled cortical impact as an experimentalmodel of TBI. Functionally, this model of TBI results in deficits offine motor coordination (as evidenced by a beam walk test), andhippocampal deficits with reduced spatial learning in a Morris watermaze test. MRI assessment of the damage showed extensive lesionsspreading from the cortex through the hippocampus and connecting to thelateral ventricles. However, injured mice lacking beta-secretase(Bace1-/-) lost less than 7% of hippocampal tissue compared to 65% lossfor mice containing beta-secretase (Bace1+/+). Pharmacologicalinhibition of gamma-secretase also reduces post-traumatic tissue lossand improves cognitive and motor recovery after trauma. Since thegamma-secretase inhibitor was administered after trauma, it models aclinically relevant situation. 379.

Country/Region

USA