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News in Brief
The cause of Parkinson’s disease (PD) remains unknown despite the fact that it is one of the most common neurological diseases. Because most people with PD do not have a family member with the disease, it is assumed that genetic factors are not the main culprit in most cases. This has led scientists to speculate that perhaps the disease is caused by something in the environment or that maybe there is something in certain environments that contributes to PD in susceptible individuals.
Scientists have long suggested that Parkinson’s may, in some cases, be caused by exposure to a specific environmental toxin, such as pesticides, including herbicides used to kill weeds and plants. Two recent reports provide more evidence for this theory.
PD Linked to Pesticide Levels in Blood
According to a new study published in the July issue of Archives of Neurology, people with Parkinson’s disease have considerably higher blood levels of a certain class of pesticide than do healthy individuals, or people with Alzheimer’s disease.
Researcher Dwight C. German, Ph.D., and his colleagues at the University of Texas Southwestern Medical Center and Robert Wood Johnson Medical School detected an association between PD and a family of pesticides called organochlorines. Organochlorines, which were used by farmers in the US from the 1950s until the 1970s, are harmful to the brain. These pesticides are specifically toxic to the brain’s dopamine cells, the site of disease in PD.
In this case-controlled study, Dr. German and colleagues collected blood samples from 50 people with Parkinson’s, 43 normal controls and 20 people with Alzheimer’s disease, between 2002 and 2007. The researchers tested all of the blood samples for 16 different kinds of organochlorines and found a disproportionately high representation of one specific pesticide, called beta-hexachlorocyclohexane (beta-HCH) in people with Parkinson’s. The controls and individuals with Alzheimer’s also had detectable levels of the pesticide in their blood, but not to the same extent as the people with PD.
Dr. German’s findings mirror those of a 2005 study in the Danish Faroe Islands, which are located off the coast of Scotland, where an island population was exposed to organochlorine pesticides and had an increased risk of PD. Although the results of these two small studies are not strong enough to prove that PD is caused by beta-HCH, it does lay the foundation for further study of this pesticide, perhaps uncovering why dopamine cells degenerate in PD.
IOM Reports on Veterans, Agent Orange and PD
In a second report, the Institute of Medicine (IOM), a component organization of the National Academy of Sciences, presented results from its biennial review of the health effects of herbicide exposure among Vietnam veterans.
For nearly a decade, between 1962 and 1971, the US military sprayed herbicides over Vietnam to reduce the jungle canopy, to clear vegetation from base camps and to destroy crops. The main chemical mixture was Agent Orange, but there were several other compounds and toxic contaminants. Since 1994, the IOM has been studying the long-term health effects of exposure to Agent Orange and other herbicides.
In the most recent report from the IOM, named the 2008 Update, there is new information from recent epidemiological studies supporting a limited association between herbicide exposure and the development of PD in Vietnam veterans. However, the biological mechanism by which two herbicides used in Vietnam, known respectively as 2,4-D and 2,4,5-T, including the dioxin contaminant of Agent Orange called TCDD, has not been conclusively demonstrated.
But if a strong association between a specific Agent Orange toxin and PD can be found, such a finding could lead to a better understanding of how PD is caused.
These two reports, one focused on blood levels of the pesticide beta-HCH and the other on epidemiological studies of herbicide exposure, do not provide conclusive evidence that any environmental factor, alone, can cause PD. But they do demonstrate statistical associations between certain toxic compounds and PD, and these need to be investigated further.
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Scientists have found a potential mechanism for rescuing the neurons that are lost in Parkinson’s disease (PD), according to an article published in the July 13 issue of Nature Chemical Biology. While the research is in its very early stages, using yeast and small worms, in the future it could suggest novel therapeutic options for people living with PD.
The team led by Joshua A. Kritzer, Ph.D., of Whitehead Institute for Biomedical Research, working in the lab of Susan Lindquist, Ph.D., looked for a way to compensate for the accumulation of alpha-synuclein that occurs in Parkinson’s. The accumulation of this protein in neurons reflects the disease process of PD, and leads to the formation of abnormal protein clumps, named Lewy bodies, within dopamine cells. Alpha-synuclein is thought to be toxic, leading to the damage and death of neurons. Past research has shown that when animal brain cells produce large amounts of alpha-synuclein, the cells die.
Using molecular genetic techniques, Dr. Kritzer and his team created an experimental model of yeast cells that accumulate large amounts of the alpha-synuclein protein. Next, they searched for small molecules named cyclic peptides that could interrupt the process of alpha-synuclein accumulation and cell damage. The scientists screened a “library” of thousands of cyclic peptides, and discovered two that had the ability to rescue the yeast cells from the effects of alpha-synuclein. Next, the team, in collaboration with Kim A. Caldwell, Ph.D., and Guy A. Caldwell, Ph.D., at the University of Alabama, Tuscaloosa, tested the same method in a more complex system than yeast: a small worm called C. elegans. They found that the same two peptides protected dopamine neurons from the toxic effects of alpha-synuclein.
Team members do not yet understand how these small proteins block the harmful effects of alpha-synuclein, but they are currently investigating it.
Pending further study, the two cyclic peptides identified in the study may indicate a novel approach for slowing or stopping the progression of Parkinson’s. In addition, the method that was used to find them represents a potentially new and efficient way to identify therapeutics not only for Parkinson’s, but for other neurodegenerative diseases as well.
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