Principal Investigator:
Nicholas D. Schiff, Professor of Neuroscience
Background & Unmet Need
- Loss of organized sleep electrophysiology is a characteristic finding after severe brain injury
- Acquired cognitive deficits may lead to loss of autonomy and independence and significantly impact patient quality of life
- Recent studies have implicated daytime brain activation as a modulator of sleep architecture in the severely injured brain
- Unmet Need: Novel therapeutics for patients who experience continued cognitive deficits following brain injury
Technology Overview
- The Technology: Treatment of acquired cognitive deficits through upregulation of GABAB signaling
- The Discovery: Administration of sodium oxybate (SO) in mice right before sleep generated an increase in the delta oscillations (1-4Hz) LFP power in the non-REM
- Administration of SO at night increased beta (20-40Hz) and gamma (>40Hz) LFP during the subsequent wakeful period
- An increase in beta and gamma frequency power is associated with the recovery of complex behaviors in a wakeful state
Technology Applications
- Treatment of cognitive deficits following brain injury, or in association with chronic disease or psychiatric disturbance
- Improvement of wakeful function
Technology Advantages
- Upregulation of GABAB signaling at night may be coupled with anterior-forebrain stimulating therapy when the subject is awake
- Several upregulators of GABA signaling are already approved for other indications (e.g., baclofen, tiagabine, zolpidem, midazolam)
Publications
Resources
Intellectual Property
Patents
- PCT Application Filed
Cornell Reference
- 8839
Contact Information
For additional information please contact
Louise Sarup
Associate Director, Business Development and Licensing
Phone: (646) 962-3523
Email: lss248@cornell.edu