Collaborators in the UA-led study were Drs. Xandra O. Breakefield and her colleagues at Harvard and Yuqing Li and his colleagues at The University of Alabama at Birmingham, known as UAB. Dr. Songsong Cao, a former doctoral student in the Caldwell Lab, is the study's lead author; two UA doctoral students, Alexander J. Burdette and Pan Chen; and one former UA student, Amber Clark Buckley, are among the co-authors.
Furthermore, the research shows ampicillin enhances the capacity of torsinA to protect, within animal models, the neurons which produce dopamine from dying. The death of these neurons in human brains leads to the hallmark symptoms of Parkinson's disease.
In a statement accompanying the paper, the researchers caution against the long-term use of an antibiotic in disease treatment.
"We have taken ampicillin and used that as a base structure to find things that work like ampicillin but which aren't ampicillin," Guy Caldwell said. "Finding molecules that are not antibiotic and still have the capacity to activate torsinA has been an ongoing effort of our lab, and we have some exciting leads in that direction."
UA filed patents covering the use of antibiotics and other novel chemicals as activators of torsinA for treatment of dystonia and other diseases, including Parkinson's disease. The University has also entered into a collaborative research and licensing agreement with QRxPharma, a clinical stage pharmaceutical company, to identify, develop and commercially exploit new torsinA activator drugs.
The UA/QRxPharma research program is directed at re-engineering existing drug therapies for new clinical applications and identifying new drug candidates for uses including the treatment of dystonia, Parkinson's disease and other neurolog
|Contact: Kristy Kain|
The Company of Biologists