Smoking, coffee intake, and Parkinson's disease: Potential protective mechanisms and components.

Simple item page
dc.citation.volume106
dc.contributor.authorHong SW
dc.contributor.authorPage R
dc.contributor.authorTruman P
dc.coverage.spatialNetherlands
dc.date.accessioned2025-01-13T01:39:31Z
dc.date.available2025-01-13T01:39:31Z
dc.date.issued2024-12-20
dc.description.abstractParkinson'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.
dc.description.confidentialfalse
dc.edition.editionJanuary 2025
dc.format.pagination48-63
dc.identifier.author-urlhttps://www.ncbi.nlm.nih.gov/pubmed/39701424
dc.identifier.citationHong SW, Page R, Truman P. (2024). Smoking, coffee intake, and Parkinson's disease: Potential protective mechanisms and components.. Neurotoxicology. 106. (pp. 48-63).
dc.identifier.doi10.1016/j.neuro.2024.12.003
dc.identifier.eissn1872-9711
dc.identifier.elements-typejournal-article
dc.identifier.issn0161-813X
dc.identifier.piiS0161-813X(24)00153-0
dc.identifier.urihttps://mro.massey.ac.nz/handle/10179/72358
dc.languageeng
dc.publisherElsevier B.V.
dc.publisher.urihttps://www.sciencedirect.com/science/article/pii/S0161813X24001530
dc.relation.isPartOfNeurotoxicology
dc.rights(c) 2024 The Author/s
dc.rightsCC BY 4.0
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectCatechol O-methyltransferase
dc.subjectCoffee drinking
dc.subjectMonoamine oxidase B
dc.subjectParkinson’s disease
dc.subjectPhenolic compounds
dc.subjectSmoking
dc.titleSmoking, coffee intake, and Parkinson's disease: Potential protective mechanisms and components.
dc.typeJournal article
pubs.elements-id492811
pubs.organisational-groupOther
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