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  Newswise — Scientists at the Buck Institute for Age Research have shown that 
combining two environmental toxic substances accelerated age-related 
degeneration in neurons associated with Parkinson’s disease (PD) in mice. 
Additionally, the study showed that pre-treating the mice with an antioxidant 
weakened the impact of the environmental exposures, suggesting the substances 
damage the neurons via oxidative stress. The toxics involved include 
increased neonatal iron intake and exposure to the herbicide paraquat. 
Results of the study were published in the June 27 issue of The Journal of 
Neuroscience. 
The study highlights the role of environmental factors in the development of 
PD, a progressive, incurable neurodegenerative disorder that results in 
tremor, slowness of movement and rigidity. Only five percent of the 160,000 
cases of PD diagnosed in the U.S. each year are strictly genetic in nature; 
most of those afflicted have “sporadic” PD, likely due to a combination of 
environmental exposures and increased genetic susceptibilities. “Research 
keeps pointing to Parkinson’s disease as being a very complex disorder,” said 
Buck Institute faculty member Julie K. Andersen, lead author of the 
study. “This research looked at environmental risk factors in the context of 
aging which is essential, given the fact that aging is the single major risk 
factor for PD in humans.”
Andersen and her team worked with genetically identical mice, which put all 
the animals on the same footing in regards to genetic susceptibility. One 
group was given an excess of iron in infancy, another was given the herbicide 
paraquat, (both compounds have been shown to increase the risk of PD in 
earlier studies in mice), a third group was exposed to both substances and a 
fourth group was not exposed to either of the compounds. Half of each group 
received treatment with the antioxidant EUK-189, which is known to cross the 
blood brain barrier. The animals in each group were aged to the human 
equivalent of young adult, young middle-age (45 – 55 in humans), young-older 
(65 – 70 and elderly (85+). Results showed that exposing animals to both 
substances accelerated PD-like neurodegeneration in the mice, with symptoms 
beginning to appear at the human equivalent of middle-age. The mice 
demonstrated a progression of increased oxidative stress followed by 
decreased neuronal function and finally neuronal cell loss. In elderly mice, 
cell loss was roughly equivalent to that observed in the human disorder. 
Those mice treated with the antioxidant, which was delivered at the same time 
as the environmental toxin, had significantly less nerve death in the area of 
the brain commonly affected by PD. 
“The fact that the antioxidant treatment prevented much of the nerve damage in 
the mice points to the need for an early diagnostic test for Parkinson’s 
disease,” said Andersen. “Currently, by the time humans are diagnosed with 
the disease they have already lost 60% of the neurons implicated in PD; 
treatment with an antioxidant would likely be maximally effective if taken 
before symptoms appear in order to halt disease progression.” 
J. Timothy Greenamyre, MD, PhD, Professor of Neurology at the University of 
Pittsburgh commented on the work, “This study provides further confirmation 
that ‘innocuous’ early life events or exposures can lead to late life 
neurodegeneration. Secondly, it adds to the evidence that that abnormalities 
of iron handling can contribute to the pathogenesis of PD.” He added, “It 
also shows that early life exposures can predispose to or exacerbate 
neurodegeneration caused by subsequent exposures.” 
Joining Andersen in the study were Jun Peng, and Fang Feng Stevensen, also of 
the Buck Institute, along with Li Peng of the Royal Perth Hospital, Perth, 
Australia; and Susan R. Doctrow of Proteome Systems, Inc., Woburn, MA. The 
work was funded by the National Institute of Environmental Health Sciences as 
part of a large Collaborative Centers for Parkinson’s Disease Environmental 
Research (CCPDER) U54 grant. 
The Buck Institute is an independent non-profit organization dedicated to 
extending the healthspan, the healthy years of each individual’s life. The 
National Institute of Aging designated the Buck a Nathan Shock Center of 
Excellence in the Biology of Aging, one of just five centers in the country. 
Buck Institute scientists work in an innovative, interdisciplinary setting to 
understand the mechanisms of aging and to discover new ways of detecting, 
preventing and treating age-related diseases such as Alzheimer’s and 
Parkinson’s disease, cancer, stroke, and arthritis. Collaborative research at 
the Institute is supported by genomics, proteomics and bioinformatics 
technology.

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