Abstract
Parkinson’s disease (PD) is a progressive neurodegenerative disorder. Genetic modifiers, environmental factors and gene–environment interactions have been found to modify PD risk and disease progression. The objective of this study was to evaluate the association of smoking, caffeine and anti-inflammatory drugs with age at onset (AAO) in a large PD cohort. A total of 35,963 American patients with idiopathic PD (iPD) from the Fox Insight Study responded to health and lifestyle questionnaires. We compared the median AAO between different groups using the non-parametric Mann–Whitney U test. Non-parametric Spearman’s correlation was used for correlation assessments and regression analysis was used to assess interaction between variables. We found that smoking (p < 0.0001), coffee drinking (p < 0.0001) and aspirin intake (p < 0.0001) show an exploratory association with AAO in PD, that was further supported by multivariate regression models. The association of aspirin with PD AAO was replicated in another cohort (EPIPARK) (n = 237 patients with PD).
Highlights
Parkinson’s disease (PD) is a progressive neurodegenerative disorder, characterized by dopaminergic neuronal loss in the substantia nigra and the presence of Lewy Bodies [1, 2]
Investigation of possible smoking dosage effects on age at onset (AAO) showed that the number of cigarettes per day was associated with later AAO (n = 4399, r = 0.08, p < 0.0001) (Fig. 1B), despite a small correlation strength
We found an association between the general intake of aspirin, number of pills per week and aspirin intake duration with later AAO
Summary
Parkinson’s disease (PD) is a progressive neurodegenerative disorder, characterized by dopaminergic neuronal loss in the substantia nigra and the presence of Lewy Bodies [1, 2]. It is the second-most common neurodegenerative disorder and the fastest-growing neurological disease currently affecting over 7 million patients worldwide [3]. A phenomenon in PD is variable age at onset (AAO) that is considered a consequence of genetic and environmental factors. Tobacco use and smoking are already known protective factors for PD risk [4–6]. Research on AAO is not as extensive.
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