Abstract

It’s well known that smoking cigarettes is causally linked to a number of serious mortal diseases. These include laryngeal, lung, bladder, and digestive tract cancers, chronic obstructive pulmonary disease and a number of cardiovascular diseases, such as aortic aneurysm, stroke, and ischemic heart disease. In 2014, U.S. Surgeon General Report states that smoking is causally associated with inflammation and impaired immune function, and that regular smokers are at higher risk of developing pneumonia, tuberculosis, and other airway infections. So the best way to avoid harm from smoking is to never start, and for smokers to quit. However, evidence from epidemiological studies suggests a relationship between cigarette smoking and low risk of Parkinson’s disease. As a major component of tobacco smoke, nicotine has been proposed to be a substance for preventing against Parkinson’s disease risk, with a key role in regulating striatal activity and behaviors mediated through the dopaminergic system. Another data suggests quick deterioration and disease exacerbation after smoking cessation. Animal studies also showed that nicotine could modulate dopamine transmission and reduce levodopa-induced dyskinesias. Smoking cessation, proposed because of the health issues as certainly reducing the risk of cardiovascular events and cancer, must be definitely accepted as major health paramount procedure, but in the case of Parkinson’s disease nicotine-substitute supplements must be provided. As a small amount of nicotine can saturate a substantial portion of nicotine receptors in the brain, nicotine from other sources, such as less harmful smoking advanced devices as well as diet, could be a promising therapeutic substance for motility support and protection against Parkinson’s disease.

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