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Natural Toxins: Their Roles In Developing PD

December 5, 2012

Dr. Mohamed Salama
Head of Experimental Neurology Unit
MERC, Mansoura University,

In rural living, individuals are exposed to variable environmental natural compound that have the ability to induce dopaminergic neuronal damage. Various epidemiological data suggested the potential role of these natural compounds to induce Parkinsonism (Caldwell et al., 2009). Epidemiological studies suggest that the prevalence of Parkinsonism is not affected by the industrial revolution. Moreover, it seems that pesticides exposure is not linked with PD prevalence. A finding that is supported by the failure of most of the synthetic toxins induced PD models to recapitulate the exact pathological features of the disease (Trimmer and Bennett, 2009). So, a new direction of using “natural” toxins in the modeling of Parkinsonism seems attractive. The success of these toxins to induce dopaminergic neuron death and protein aggregation in vitro led us to think of them as new candidates that could be able to improve animal models of Parkinsonism (Shen et al., 2010).

Inhibition of complex I of the mitochondrial respiratory chain has also been implicated in the pathophysiology of PD (Schapira et al., 1990). Many toxins of herbal, microbial or synthetic origin can induce neuronal cell death in cultured neurons in vitro (Höllerhage et al., 2009). The success of new environmental toxins to develop mitochondrial complex I inhibition and degeneration of dopaminergic neurons in vitro (Arif and Khan, 2010), coupled with epidemiological data suggesting natural environmental toxin involvement in Parkinsonism pathogenesis would invite us to think of these natural toxins as new candidates for developing models (Tanner, 2010).

The choice of certain natural toxins for PD modeling needs some guidelines as supposed by Shaw and Hoeglinger [2008].

1. The agent must be of natural origin.
2. The agent must be available worldwide to contribute to the wide prevalence of PD in
the whole world.
3. The agent must recapitulate PD pathology in experimental animals.

We are trying to explore the role of various natural agents, able to inhibit complex I, in developing PD in animals. This work is carried in Experimental Neurology Unit, MERC, Mansoura University. Defining possible agents can help in many aspects; first we will be able to develop invivo model that can recapitulate the pathological findings in PD. Moreover, we will be able to identify high risk population exposed to these factors.


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