Researchers have discovered that low doses of carbon monoxide, similar to levels experienced by smokers, can protect against neurodegeneration in Parkinson’s disease models. The study found that carbon monoxide reduced the accumulation of the Parkinson’s-associate protein alpha-synuclein and activated pathways that limit oxidative stress.
These findings suggest that molecular mechanisms triggered by low-dose carbon monoxide could slow the progression of Parkinson’s disease. A clinical trial to test this therapy in Parkinson’s patients is being planned.
The research, published in npj Parkinson’s Disease, used rodent models of Parkinson’s disease based on alpha-synuclein accumulation and oxidative stress. The study found that oral administration of a low dose of carbon monoxide mitigated neurodegeneration and reduced alpha-synuclein pathology.
Mechanistically, the researchers showed that low-dose carbon monoxide activated signaling pathways that limit oxidative stress and degrade alpha-synuclein. This suggests that carbon monoxide may slow the onset and limit the pathology in Parkinson’s disease.
The team also found that heme oxygenase-1 levels were higher in the cerebrospinal fluid of people who smoke compared to nonsmokers, and in brain tissue samples from patients with Parkinson’s, heme oxygenase-1 levels were higher in neurons that were free of alpha-synuclein pathology.
Source: https://neurosciencenews.com/parkinsons-smoking-neurology-27633/