ve made considerable progress in the development of MAO B inhibitors to treat neurodegenerative and psychiatric disorders, we are very optimistic that our new knowledge about the three-dimensional structure of the enzyme will facilitate additional improvements in drug design which will lead to increased specificity and fewer side effects," said Dale Edmondson, Ph.D., professor of biochemistry, Emory University School of Medicine, and co-principal investigator of the project .

Other authors included co-principal investigator Andrea Mattevi, Department of Genetics and Microbiology, University of Pavia and postdoctorals Claudia Binda, Paige Newton-Vinson and Frantisek Hubalek.

MAO B has been shown to be elevated more than three fold in the brain tissue of elderly individuals. Recent studies have shown that elevated levels of MAO B in neurons and kidney cells can lead to cell death (apoptosis). Clinical trials currently are underway in several centers to target increased levels of MAO B that have been identified in astrocytes (a type of brain cell) in Alzheimers patients.

"The structural insights will provide us with a new framework to explore the catalytic mechanism of the enzyme, to understand the differences between the A and B forms, and to design specific new inhibitors to treat and prevent age-related disorders," Dr. Edmondson said. "It also will help us understand the role of these enzymes in the clearance of amine-containing drugs either in development or in clinical use for the treatment of other disorders."

"This finding may well result in the development of novel treatments for depression a major public health problem," said Charles Nemeroff, M.D., Ph.D., Reunette W. Harris professor of psychiatry and behavioral sciences at Emory University School of Medicine and chair of the department. "MAO inhibitors are excellent antidepressants but have an unfavorable side-effect profile. This discovery should allow for the s
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Contact: Holly Korschun
hkorsch@emory.edu
404-727-3990
Emory University Health Sciences Center
25-Nov-2001

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