Protection by 1-deprenyl (-DEP) a selective MAO-B inhibitor against MPTP- parkinsonism has been attributed to the inhibition of conversion of MPTP of MPP+ catalyzed by MAO-B. Recent results demonstrate that: 1) 30-min post-treatment by -DEP, but not pargyline prevents MPTP-induced striatal DA depletion (Sziraki et al., 1991) DEP promote the survival of dopaminergic neurons when applied 3 days after MPTP. 2.) -DEP decreases hydroxyl radical formation elicited by 2'methyl-MPTP or MPP+ (Chiueh, et al., 1992, Wu et al., 1993), (Tatton and Greenwood, 1992), clearly indicating that factors other than blocking the formation of MPP+ are also involved in dopaminergic neuroprotection by -DEP. My objective during the period of award is to further investigate the novel neuroprotective and neurorescue effect of -DEP and the underlying mechanisms in the framework of collaborative projects with Dr. C. C. Chiueh. Getting familiar with new techniques in molecular pharmacology and molecular biology would enhance my research skills and my understanding of neurodegenerative disorders which is of primary importance in my long-range carrier plans.

Agency
National Institute of Health (NIH)
Institute
Fogarty International Center (FIC)
Type
International Research Fellowships (FIC) (F05)
Project #
1F05TW005131-01
Application #
2293194
Study Section
Special Emphasis Panel (NSS)
Project Start
1994-11-14
Project End
Budget Start
1994-06-01
Budget End
1995-05-31
Support Year
1
Fiscal Year
1994
Total Cost
Indirect Cost
Name
U.S. National Institute of Mental Health
Department
Type
DUNS #
623156465
City
Bethesda
State
MD
Country
United States
Zip Code
20892