Peppers have also been recommended

(Susan Searles Nielsen et al.)

http://www.sciencedaily.com/releases/2013/05/130509091215.htm

http://onlinelibrary.wiley.com/doi/10.1002/ana.23884/abstract

Other literature:

http://medicalxpress.com/news/2011-08-up-side-nicotine-brain-parkinson-disease.html

http://onlinelibrary.wiley.com/doi/10.1002/ana.20307/full

http://www.eurekalert.org/pub_releases/2007-04/jaaj-sac040507.php

http://www.newscientist.com/article/dn18814-parkinsons-protection-without-caffeine-or-nicotine.html

Regards,

Joachim (not an expert)

Two constituents in tobacco leaves implicated in this protective effect are nicotine, a free radical scavenger, and MAO inhibitors {Castagnoli & Murugesan 2004 #14535}{Moore, Huckerby, et al. 2004 #14613}. Nicotine is the most conspicuous constituent of cigarette tobacco and smoke {Castagnoli & Murugesan 2004 #14535}. Moore et al. {Moore, Huckerby, et al. 2004 #14613} used nuclear magnetic resonance to show that both D and L enantiomers of nicotine inhibit protein aggregation, a mechanism implicated in PD pathogenesis. [Nicotine also acts as a nicotinic receptor antagonist and may have a neuroprotective effect in the 6-OHDA model of PD {Ryan, Ross, et al. 2001 #14763} Moreover, nornicotine, a major nicotine metabolite in brain that forms Schiff-base adducts with aldehydes, blocks protein aggregation including β-amyloid {Dickerson & Janda 2003 #2423} and -synuclein (Prelim. Results, Fig. 7D).]. Both tobacco leaf extracts and cigarette smoke contain reversible and irreversible MAO-A and MAO-B inhibitors {Castagnoli & Murugesan 2004 #14535}. Fowler et al. {Fowler, Volkow, et al. 1996 #14597} measured MAO-B levels in the brains of living smokers using positron emission tomography and deuterium substituted deprenyl, a radiotracer which binds irreversibly to MAO-B. They showed a 40% decrease in the level of MAO-B levels in the brains of living smokers relative to either non-smokers or former smokers. In further studies Fowler et al. {Fowler, Volkow, et al. 1996 #14609} demonstrated inhibition of MAO-A in brains of cigarette smokers. Castagnoli et al. {Castagnoli & Murugesan 2004 #14535} identified an MAO-B inhibitor in tobacco leaf extracts as 2,3,6-trimethyl-1,4-naphthoquinone (TMN), also present in cigarette smoke. They showed that TMN provides neuroprotection in the MPTP mouse model of PD. [We propose to investigate the role that free radical scavengers (e.g., nicotine), nicotinic receptors, Schiff-base adduct formation (e.g., nornicotine) or MAO inhibitors have on DOPAL-induced death of dopaminergic neurons in the rat brain.]