Effects of nicotine on motor deficits and lifespan when given on different treatment days in a Parkinson's disease model. Mukul Mallick¹, Lori M. Buhlman¹, Gerald B. Call². 1) Biomedical Sciences, Midwestern University, Glendale, AZ; 2) Dept. of Pharmacology, Midwestern University, Glendale, AZ.

   In the US, Parkinsons disease (PD) affects about 13 out of 100,000 and is the second leading neuromotor degenerative disease (Van Den Eeden et al., 2002). Drosophila melanogaster with parkin loss-of-function mutation exhibit similar pathology to patients with familial PD such as motor deficits, mitochondrial pathology and decreased lifespan, which makes it especially viable as a model for familial PD compared to other parkin loss-of-function models, which do not exhibit these symptoms. Motor deficits may stem from mitochondrial pathology, which leads to indirect flight muscle degeneration (Greene et al., 2003). Epidemiological studies suggest a delay in the onset of PD in tobacco smokers (Hernan et al., 2001; Grandinetti et al., 1994; Rajput et al., 1987) and that nicotine has neuroprotective effects in models of sporadic PD (reviewed in Quik et al., 2009). Previous data in our lab suggests that nicotine rescues motor, viability and loss of olfaction symptoms in +/park²⁵ D. melanogaster when given at day one post eclosion. This study was initiated to determine if nicotine can rescue symptoms when administered at later days by assessing climbing and flight assays on wild-type and +/park²⁵ D. melanogaster when exposed to nicotine at later days post eclosion. Initial results indicate that treatment with nicotine at 3 days post eclosion improves climbing and flight. Further details and a complete time course for nicotine administration will be presented at the meeting. These results will clarify whether nicotine can be an effective treatment for familial PD when given to patients after they first start experiencing symptoms such as loss of olfaction.