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In a message dated 27/06/2007 07:14:43 GMT Standard Time,  
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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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I've suspected for some time that my PD may've been triggered by overdoing  
the iron tablets I took the previous year to conteract anaemia caused  by very 
heavy periods - damm menopause...
 



   

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