Environmental Factor, September 2006, National Institute of Environmental Health Sciences
New Study Explores Nicotine's Potential as Protection against Parkinson's
By Eddy Ball
Researchers at the Parkinson's Institute in Sunnyvale, CA, have demonstrated that nicotine, a compound that is dangerous and addicting for most people, could prove to help some patients delay or avoid onset of Parkinson's, one of the most feared crippling conditions of our time. The five-year study found that in laboratory animals, systematic administration of controlled dosages of nicotine in sweetened drinking water significantly reduced the effects of experimentally induced Parkinson's syndrome. Published in July as an early release from the Journal of Neurochemistry, the study reports that nicotine-treated animals suffered 25 percent less damage than animals that had not received the intervention.
Because the study results appear inconsistent with public health warnings about the serious health consequences of tobacco use, medical experts have been eager to help the public put the findings into perspective. "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," commented David Schwartz, director of NIEHS, which funded the study. "These findings also have implications for its use in slowing the progression of Parkinson's," he said.
Most of the research on tobacco has focused on its detrimental health effects. However, several studies conducted over the last 40 years have shown that the incidence of Parkinson's disease is about 50 percent 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," explained Maryka Quik, Ph.D., a senior research scientist with the Parkinson's Institute and lead author on the study.
Researchers used MPTP, a known industrial toxin and a common contaminant resulting from street-lab synthesis of designer drugs, to stimulate development of Parkinson symptoms in lab animals. A rash of Parkinson-like symptoms among users of these drugs in the early 1980's pointed medical researchers to a model for studying the course of Parkinson's. Using experimental animals exposed to MPTP, Quik and her colleagues were able to isolate critical markers of physical changes in the bodies of Parkinson's patients, including nicotine receptor activity (subject of a 2004 study led by Quik) and synthesis of the neurotransmitter dopamine. Measures of these two markers showed significant differences between the test and control groups.
Neurotransmitters, such as dopamine, are the "communicators" in the body's nervous system. Disruption in the synthesis and reuptake of these important chemicals can produce serious health effects. Several medications target reuptake of the neurotransmitters serotonin and norepinephrine in patients with depression. One of the principal medications developed for Parkinson's patients acts on dopamine synthesis, but it is not effective for as many as half of the patients treated and may produce significant physical and psychological side effects for many who take it.
Medical researchers continue to look for additional ways to regulate neurotransmitter activity to treat the disease more effectively.
While Parkinson's Institute investigators called for further study with larger experimental populations and acknowledged the limitations of animal studies, they emphasized the significance of the study's results.
"Nicotine [may be effective] as a therapeutic agent for Parkinson's disease, because nicotine or selective neuronal nicotinic receptor agonists ... may counteract disease progression particularly if given during the early stages."
Citation: Quik M, Parameswaran N, McCallum SE, Bordia T, Bao S, McCormack, A, Kim A, Tyndale RF, Langston JW, Di Monte DA. 2006. Chronic oral nicotine treatment protects against striatal degeneration in MPTP-treated primates. J Neurochem on-line early release doi:10.1111/j.1471-4159.2006.04078.x