Anyone using a nicotine patch? Any opinion on its value as a "rescue" technique rather than a daily thing?

Neural Transm Suppl. 2006;(70):177-80. Links
Nicotine induces brain CYP enzymes: relevance to Parkinson's disease.

Miksys S, Tyndale RF.
Department of Pharmacology, Centre for Addiction and Mental Health, University of Toronto, Ontario, Canada.
Brain expression of cytochromes P450 2B6, 2D6 and 2E1 is higher in smokers, and is induced by nicotine in animals. These enzymes can metabolize many of the neurotoxins associated with Parkinson's disease. Since smoking is known to be protective against Parkinson's disease, we hypothesise that nicotine-induced elevation of brain CYPs in smokers may contribute to neuroprotection against Parkinson's disease. This supports the therapeutic use of nicotine to delay the progress of this disease.


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Eur J Neurosci. 2007 Jun 20
Neuroprotective effect of nicotine on dopaminergic neurons by anti-inflammatory action.

Park HJ, Lee PH, Ahn YW, Choi YJ, Lee G, Lee DY, Chung ES, Jin BK.
Department of Neurology, Ajou University School of Medicine, Suwon, Korea.
Epidemiological studies have reported that smoking is associated with a lower incidence of Parkinson's disease (PD), leading to theories that smoking in general and nicotine in particular might be neuroprotective. Recent studies suggested cholinergic anti-inflammatory pathway-regulating microglial activation through alpha7 nicotinic receptors. In the present study, we used lipopolysaccharide (LPS)-induced in vitro and in vivo inflammation models to investigate whether nicotine has a protective effect on the dopaminergic system through an anti-inflammatory mechanism. Nicotine pretreatment considerably decreased microglial activation with significant reduction of tumour necrosis factor (TNF)-alpha mRNA expression and TNF-alpha release induced by LPS stimulation. In co-cultures of microglia and mesencephalic neurons, nicotine pretreatment significantly decreased the loss of tyrosine hydroxylase-immunopositive (TH-ip) cells, approximately twice more than the LPS-only treatment. alpha-Bungarotoxin, an alpha7 nicotinic acetylcholine receptor subunit-selective blocker, considerably blocked the inhibitory effects of nicotine on microglial activation and TH-ip neuronal loss. Chronic nicotine pretreatment in rats showed that TH-ip neuronal loss induced by LPS stimulation in the substantia nigra was dramatically decreased, which was clearly accompanied by a reduction in the formation of TNF-alpha. The present study demonstrated that nicotine has a neuroprotective effect on dopaminergic neurons via an anti-inflammatory mechanism mediated by the modulation of microglial activation. Along with various neuroprotective effects of nicotine, the anti-inflammatory mechanism of nicotine could have a major therapeutic implication in the preventive treatment of PD.