The credibility of nicotine as a way of slowing the progression of PD is based in part on epidemiological studies. These have shown the there is a lower prevalence of PD amongst smokers, as opposed to non-smokers.

An old paper by Hong et. al. [1] suggests a possible causal mechanism for this result.

"nicotine and hydroquinone inhibit [alpha]-synuclein fibril formation in a concentration-dependent manner, with nicotine being more effective. The SEC-HPLC data show that nicotine and hydroquinone stabilize soluble oligomers."

The reason that this is important is that it is thought that the aggregation of alpha-synuclein plays a key role in the pathogenesis of PD.

A recent paper by Barreto et al. [2] describes a number of mechanisms in which nicotine may work. It concludes with this statement:

"Derivatives of nicotine such as cotinine have great potential to become effective agents to prevent and alleviate neurological symptoms developed in subjects with Parkinsonism. It is surprising the absence of funding for the clinical development of these compounds, as they could be therapeutic solutions which have been lying in front of our eyes for hundreds of years, waiting for development."

References

[1] Biochim Biophys Acta. 2009 Feb; 1794(2): 282–290.
"Smoking and Parkinson’s disease: Does nicotine affect alpha-synuclein fibrillation?"
Dong-Pyo Hong, Anthony L. Fink, and Vladimir N. Uversky
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2647853/

[2] Front. Aging Neurosci., 09 January 2015 |
"Beneficial effects of nicotine, cotinine and its metabolites as potential agents for Parkinson’s disease"
George E. Barreto, Alexander Iarkov2,3 and Valentina Echeverria Moran
http://journal.frontiersin.org/artic...014.00340/full

John