Smoking, which is pointed out as a major cause of health deterioration along with alcohol, has consistently been shown to paradoxically lower the risk of developing Parkinson’s disease. However, the reason has not been clear until now.
Researchers at Massachusetts General Hospital, affiliated with Harvard Medical School in the United States, have discovered that low-dose carbon monoxide inhaled when smoking helps prevent neurodegeneration and the accumulation of key proteins associated with Parkinson’s disease in the brain.
Parkinson’s disease, which legendary boxer Muhammad Ali suffered from in his later years, is a central nervous system disease that causes movement disorders such as muscle stiffness, tremors, and slow movements due to the loss of dopamine-producing cells in the brain area that controls movement.
The number of Parkinson’s disease patients worldwide is estimated at about 10 million, and the number of patients in Korea is estimated at about 150,000.
“Because smoking has been consistently linked to a reduced risk of Parkinson’s disease, we wondered what components in cigarette smoke might provide the neuroprotective effect,” said first author Dr. Stephen Gomperts, a physician at Massachusetts General Hospital and associate professor of neurology at Harvard Medical School.
“One of the reasons we focused on carbon monoxide is because it is produced endogenously in response to stress and has been shown to have protective properties at low levels,” Dr. Gomperts said. “Additionally, overexpression of hemooxygenase-1, a stress-induced enzyme that produces carbon monoxide, has been shown to protect dopaminergic neurons from neurotoxicity in animal models.”
According to a report in Harvard Gazette on the 28th (local time), nicotine, another major component of cigarette smoke, was found to be ineffective in slowing the progression of the disease in a recently published clinical trial. Accordingly, Dr. Gomperts and colleagues examined the relationship between carbon monoxide and Parkinson’s disease in an experiment using mice.
The researchers administered low doses of carbon monoxide in oral drug form to mice, at doses similar to those experienced by smokers. They found that carbon monoxide protected mice from disease-causing factors, including loss of dopaminergic neurons and accumulation of alpha-synuclein, a protein associated with Parkinson’s disease, in neurons. Mechanistically, low doses of carbon monoxide activated signaling pathways that limit oxidative stress and break down alpha-synuclein.
The researchers also found that smokers had higher levels of heme oxygenase-1 (HO-1) in their cerebrospinal fluid compared to non-smokers. In addition, in brain tissue samples from Parkinson’s patients, HO-1 levels were higher in neurons without alpha-synuclein pathology.
“These findings suggest that molecular pathways activated by low-dose carbon monoxide may slow the onset of Parkinson’s disease and limit its pathology,” Dr. Gomperts said. “They also support the need to investigate whether low-dose carbon monoxide and the pathways it modifies may slow disease progression.”
The researchers said they are planning a clinical trial of low-dose oral carbon monoxide in patients with Parkinson’s disease.
This study was published last week in ‘NPJ Parkinson’s Disease’, an international academic journal published by Nature.
Reporter Park Hae-sik, Donga.com [email protected]
-
- great
- 0dog
-
- I’m sad
- 0dog
-
- I’m angry
- 0dog
-
- I recommend it
- dog
Hot news right now
2024-08-31 02:09:31