Nicotine-Dependent Risk Of Developing Parkinson’s Disease

Abstract

For the past twenty years, information concerning the relationship between Parkinson’s disease and the use of tobacco products has appeared in highly respected scientific publications. As a whole, these studies were epidemiological. As a rule, these studies showed that individuals who abused tobacco products for many years and quit smoking only in old age had a significantly increased risk of developing Parkinson’s disease. Only a few studies have attempted to identify the structural-functional relationship between the effects of nicotine on the representative brain areas responsible for the onset of Parkinson’s disease. During prolonged tobacco use, nicotine that enters the brain tissue activates the nicotine-dependent acetylcholine receptors localized in dopaminergic neurons, resulting in the release of dopamine. In this study, we attempted to investigate the mechanisms underlying the onset of Parkinson’s disease in individuals who have quit smoking, i.e. under conditions of nicotine withdrawal in the brain.” In our opinion, the “preventive effect” of nicotine on dopaminergic neurons is realized through four interdependent mechanisms: 1. By the receptor mechanism, due to the nicotine-dependent acetylcholine receptors located on dopaminergic neurons, 2. Due to the balanced release and reuptake of dopamine to dopaminergic neurons, 3. Due to prevention of α-synuclein aggregation and fibrillation process, 4. Due to the inhibitory effect of nicotine on the processes of activating the synthesis of aliphatic polyamines in dopaminergic neurons of the corpus striatum and nucleus caudatum. In cases of nicotine “deficiency”, neurodegenerative disorders pathognomonic for Parkinson’s disease can occur in the brain: 1. The exchange of dopamine and aliphatic polyamines in dopaminergic neurons is disturbed, 2. The processes of transforming native α-synuclein into its aggregated and fibrillar forms are intensified, 3. Ultimately, the intraneuronal dopamine-synuclein complex with a pronounced neurotoxic action spectrum may appear. 4. Older adults, in conditions of abrupt smoking cessation, are recommended to use Eflornithine, as well as a polyamine-free and polyamine-deficient diet.