Large-scale prospective cohort data from the China Kadoorie Biobank reveal an inverse association between smoking and Parkinson’s disease (PD) risk, despite smoking’s known harms.
Higher exhaled carbon monoxide (CO) levels among never-smokers correlate with reduced PD incidence, suggesting a protective effect of CO independent of tobacco exposure.
Emerging mechanistic studies implicate oxidative stress modulation, mitochondrial function, and dopaminergic metabolism as plausible biological pathways linking CO and neuroprotection in PD.
These findings support ongoing clinical trials investigating therapeutic CO administration for PD, highlighting a novel translational treatment avenue.
Background
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