患帕金森病的尼古丁依赖风险

A. Zilfyan, S. Avagyan
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摘要

在过去的二十年里,关于帕金森氏症与烟草制品使用之间关系的信息出现在备受尊敬的科学出版物中。总的来说,这些研究是流行病学的。一般来说,这些研究表明,滥用烟草制品多年,直到老年才戒烟的人患帕金森病的风险明显增加。只有少数研究试图确定尼古丁对负责帕金森病发病的代表性大脑区域的影响之间的结构-功能关系。在长时间吸烟的过程中,进入脑组织的尼古丁激活了多巴胺能神经元中尼古丁依赖的乙酰胆碱受体,导致多巴胺的释放。在这项研究中,我们试图调查戒烟者帕金森病发病的机制,即在大脑中尼古丁戒断的情况下。”我们认为尼古丁对多巴胺能神经元的“预防作用”是通过四个相互依赖的机制来实现的:1。通过受体机制,由于尼古丁依赖的乙酰胆碱受体位于多巴胺能神经元上,2。由于多巴胺能神经元的释放和再摄取平衡,由于阻止α-突触核蛋白聚集和纤颤过程,由于尼古丁对激活纹状体和尾核多巴胺能神经元中脂肪族多胺合成的过程有抑制作用。在尼古丁“缺乏”的情况下,帕金森病的典型症状神经退行性疾病可能发生在大脑中:多巴胺能神经元中多巴胺和脂肪多胺的交换受到干扰。将天然α-突触核蛋白转化为聚集和纤维状形式的过程被加强。最终,可能出现具有明显神经毒性作用谱的神经元内多巴胺-突触核蛋白复合物。4. 在突然戒烟的情况下,建议老年人使用依氟鸟氨酸,以及无多胺和缺乏多胺的饮食。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nicotine-Dependent Risk Of Developing Parkinson’s Disease
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.
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