# Progress and Prospects in Parkinson's Research/Causes/Toxins

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## Toxins

A growing number of toxic compounds have been found which can, following exposure, induce the symptoms of Parkinson's Disease. Research into PD-related toxins can have a number of benefits.
* It can enable environmental hazards to be identified and eliminated.
* It can provide explanations for clustered occurrences.
* It can enable the identification of people at risk.
* It can provide a starting point for the study of the pathogenesis of the disease.
* It can provide a means whereby the disease can be reproduced under laboratory conditions.
* It will enable the improved diagnosis and treatment of cases previously classed as Atypical, Sporadic or Idiopathic.
It is not easy to prove the effects of a toxin since one cannot experiment with them on human beings. However when it comes to mind-altering substances people are often inclined to experiment on themselves - sometimes with devastating consequences. These occasions have however opened windows on research.
The pages which follow have been compiled with a view to answering the following questions about candidate toxins:-
* Has the connection between the toxin and the onset of PD been established beyond reasonable doubt?
* What does the toxin do to the nervous system?
* Does PD induced by the toxin have distinctive features?
* Is the condition preventable or reversible.
* Does the toxin act as trigger for a genetic mutation?
Readers are invited to contribute additional relevant observations and references.

## Research Findings to date

2007
Chen et al evaluated the association between dairy intake and risk of Parkinson’s disease among 57,689 men and 73,175 women (USA). They found that consumption of dairy products increased the risk of getting P.D.
2010/11
Research at St.Louis University has suggested that a naturally occurring toxin called Dopal may be involved in the onset of PD.
Cannon et al gives a comprehensive review of the current state of knowledge on neurotoxins with an informative section on Parkinson’s Disease.
They suggest a subdivision of the effects of neurotoxins into two broad categories, viz:-
Acute
Where shortly after exposure — hours to days - a neurological phenotype presents. This may or may not be reversible or stem from cell loss. Exposure may interfere with neurophysiological functioning, without initiating permanent dysfunction. In such cases the symptoms may disappear when the exposure source is removed.
Chronic
Where neurotoxicant exposure requires weeks to years and, in some cases, decades to produce cell dysfunction and cell death that result in permanent detectable neurological alterations.
The authors urge caution in classifying toxin-induced PD symptoms as true manifestations of the disease:-
   These findings are often presented in the form of case reports with limited pathological data, where much further validation would be required to establish relevance to PD. Behavioral features may arise from extrapyramidal dysfunction that does not share the pathological features of PD and additional neurological features that are not characteristic of PD also may be present. Environmental exposures that significantly alter dopaminergic neurotransmission in the substantia nigra and its projections could potentially result in movement abnormalities that share some features of PD. The majority of these exposures may actually bear limited relevance to the etiology of PD.