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NICOTINE MAY PROTECT AGAINST PARKINSON’S DISEASE
 
  The protective effect may explain the lower incidence of Parkinson’s disease 
among smokers and suggests that nicotine may be useful in the treatment of 
early-stage Parkinson’s patients.
Parkinson’s disease is a progressive, neurodegenerative disease caused by the 
death of small clusters of cells in the midbrain. The gradual loss of these 
cells results in reduction of a critical transmitter called dopamine, the 
chemical messenger responsible for normal movement.
“While we would never recommend that people smoke, these results suggest that 
nicotine promotes the survival of dopamine-producing cells in animals with no 
overt Parkinson’s symptoms,” said David A. Schwartz, M.D., director of the 
National Institute of Environmental Health Sciences, the federal agency that 
provided funding for the study. “These findings also have implications for 
its use in slowing the progression of Parkinson’s.”
Most of the research on tobacco has focused on its detrimental health effects. 
However, studies conducted over the last 40 years show that the incidence of 
Parkinson’s disease is about 50 per cent less in smokers than in the general 
population. 
“These studies were giving us clues that something in the smoke was reducing 
the incidence of Parkinson’s,” said Maryka Quik, Ph.D., a senior research 
scientist with The Parkinson’s Institute and lead author on the study.
Based on these findings, the researchers wondered what compound in cigarette 
smoke could be causing this effect. “We decided to focus our attention on 
nicotine because studies have shown that nicotine stimulates the release of 
dopamine in the brain region that is associated with Parkinson’s,” said Quik.
Results from the five-year study, conducted by researchers at The Parkinson’s 
Institute, California (USA), are published in an on-line early release in the 
Journal of Neurochemistry.
To test their theory, the researchers treated experimental animals with MPTP, 
an agent that selectively destroys the dopamine-producing brain cells. Half 
of the animals also received a low-dose administration of nicotine over a 
six-month period. During this time, the nicotine dose was gradually increased 
to a level typically found in cigarette smoke.
The test results showed that animals receiving only the MPTP suffered a 75 
percent loss of function in their dopamine-containing brain cells. When the 
researchers tested the animals that had received both MPTP and nicotine, the 
damage in the dopamine cells was only 50 per cent. “The results suggested 
that the nicotine treatment had reduced the cell damage by 25 per cent,” said 
Quik.
While there is no immediate explanation for this effect, the researchers 
believe the nicotine may stimulate the release of naturally occurring 
proteins called growth factors that play a key role in nerve cell growth and 
repair. “It is also possible that the nicotine may activate the immune system 
to protect the cells from MPTP-induced damage,” said Quik.
According to Quik, Parkinson’s disease symptoms only start to develop when 80 
to 90 per cent of dopamine in striatal nerve terminals is depleted. “This 
means that a reduction in terminal damage from 80 to 60 percent can mean the 
difference between having disease symptoms and being symptom-free,” said 
Quik.
While treatments currently available for Parkinson’s disease are limited to 
the day to day relief of symptoms, nicotine may someday be used to reduce or 
even prevent the progression of the disease. 
“With current symptomatic therapies, the progress of the disease is not halted 
and, symptoms become worse and more difficult to control,” said Quik. “With 
neuroprotection, a patient could receive treatment that would halt the 
disease progress and prevent symptoms from getting worse.”
Reference: M. Quik, N. Parameswaran, S.E. McCallum, Bordia T, Bao S, 
McCormack, Kim A, Tyndale RF, Langston JW, Di Monte DA. Chronic Oral Nicotine 
Treatment Protects Against Striatal Degeneration in MPTP-Treated Primates. 
Journal of Neurochemistry, on-line early release 
doi:10.1111/j.1471-4159.2006.04078.x

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