Abstract
Evidence from epidemiological studies suggests an association between cigarette smoking and a low risk of Parkinson’s disease. Other data indicate a rapid worsening of the disease and an exacerbation of the disease after smoking cessation. To prevent the risk of Parkinson’s disease as the main component of cigarette smoke, nicotine is proposed as a alkaloid that has a fundamental role in the regulation of the behavior and activity of the striatum mediated by the dopaminergic system. Animal studies have also shown that nicotine can regulate dopamine transmission and reduce levodopa-induced dyskinesia. However, previous clinical trials have shown conflicting results regarding nicotine treatment. Epidemiological, preclinical, clinical updates and studies on dietary nicotine are presented. The suggestion to quit smoking for health reasons, as it reduces the risk of cancer and cardiovascular disease, should be accepted as an essential health procedure, however, in the case of Parkinson’s disease, a nicotine replacement supplement should be provided. Since small amounts of nicotine can lead to stimulation of a large portion of the brain’s nicotinic receptors, nicotine from other sources, such as less harmful advanced smoking devices, as well as diet, may be promising therapeutic agents to support motor function and protect against Parkinson’s disease.
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