Hong Sa Weon, Page Rachel, Truman Penelope
School of Health Sciences, Massey University, Wellington 6021, New Zealand.
School of Health Sciences, Massey University, Wellington 6021, New Zealand.
Neurotoxicology. 2025 Jan;106:48-63. doi: 10.1016/j.neuro.2024.12.003. Epub 2024 Dec 17.
Parkinson's disease (PD) is a common progressive neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc). Environmental and lifestyle factors, such as smoking and coffee drinking, have been associated with a decreased risk for PD. However, the biological mechanisms underlying protective effects on PD are still not fully understood. It has been suggested that non-nicotine components in cigarette smoke and non-caffeine components in coffee may contribute to this protective effect. The aim of this review was to explore candidate molecules and mechanisms behind the effects of smoking and coffee drinking on PD by integrating findings from previous studies. By cross-referencing an index of tobacco constituents and a list of coffee constituents with existing literature on natural compounds and their structural analogs that show inhibitory activities against monoamine oxidase B, catechol O-methyltransferase, and α-synuclein fibrillation, we have identified tobacco and coffee components that inhibit these targets. Furthermore, tobacco and coffee components potentially play roles in suppressing neuroinflammation, activating the Nrf2 pathway as natural activators, and altering the gut microbiome. This review suggests that the phenolic compounds from tobacco and coffee investigated may contribute to the low incidence of PD in smokers and coffee drinkers, showing moderate to strong potential as therapeutic interventions. The current review suggests that multifunctional molecules found in coffee and cigarette smoke may have potential neuroprotective effects, but none of the data indicates that multifunctionality is required for these effects. This review will deepen our understanding of how smoking and coffee drinking are linked to a reduced risk of PD and will also be important in elucidating the mechanisms underlying the protective effects of smoking and coffee drinking on PD.
帕金森病（PD）是一种常见的进行性神经退行性疾病，其特征是黑质致密部（SNpc）中的多巴胺能神经元丧失。环境和生活方式因素，如吸烟和喝咖啡，与患PD风险降低有关。然而，对PD具有保护作用的生物学机制仍未完全了解。有人提出，香烟烟雾中的非尼古丁成分和咖啡中的非咖啡因成分可能促成这种保护作用。本综述的目的是通过整合先前研究的结果，探索吸烟和喝咖啡对PD影响背后的候选分子和机制。通过将烟草成分索引和咖啡成分列表与现有关于对单胺氧化酶B、儿茶酚-O-甲基转移酶和α-突触核蛋白纤维化具有抑制活性的天然化合物及其结构类似物的文献进行交叉引用，我们确定了抑制这些靶点的烟草和咖啡成分。此外，烟草和咖啡成分可能在抑制神经炎症、作为天然激活剂激活Nrf2途径以及改变肠道微生物群方面发挥作用。本综述表明，所研究的来自烟草和咖啡的酚类化合物可能是吸烟者和咖啡饮用者中PD发病率低的原因，作为治疗干预措施显示出中度至强的潜力。当前综述表明，在咖啡和香烟烟雾中发现的多功能分子可能具有潜在的神经保护作用，但没有数据表明这些作用需要多功能性。本综述将加深我们对吸烟和喝咖啡如何与降低PD风险相关联的理解，并且在阐明吸烟和喝咖啡对PD保护作用的潜在机制方面也将具有重要意义。
