http://www.ncbi.nlm.nih.gov/pubmed/22114853?dopt=Abstract
The risk of Parkinson's disease is reduced by cigarette smoking, which
raises some unanswered questions. Nicotine, a major component of
tobacco smoke, could exert either non-receptor-mediated biological
effects or, more importantly, act on the different subtypes of
nicotinic brain receptors, in particular those associated with the
nigrostriatal dopaminergic pathway. There is now robust experimental
evidence for a neuroprotective effect of nicotine upon dopaminergic
neurons. By contrast, in animal models of Parkinson's disease, nicotine
alone has slight or no motor effects. However, nicotine may modulate
dopamine transmission and has clear motor effects when associated with
L-DOPA, reducing L-DOPA-induced dyskinesias. Clinical trials have
yielded inconclusive results thus far and are hampered by different
designs and small cohorts. Ongoing studies address either symptomatic
motor or non-motor symptoms, or neuroprotection. There is still no
agreement on the daily dosage of nicotine or the method of
administration. Together, these data suggest that nicotine or nicotinic
receptor drugs have therapeutic potential for Parkinson's disease,
although the specific treatment regimens remain to be determined.
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