OLPA Hearing Report - Thimerosal/Autism

http://olpa.od.nih.gov/OLPAReports/042601AutismII.htm

Print this one out and read it carefully. Here is an excerpt:

Mercury has long been known to be a potent neurotoxic substance, whether it is inhaled or consumed in the diet as a food contaminant. Over the past fifteen years medical research laboratories have established that dental amalgum (phonetic) tooth fillings are a major contributor to mercury body burden. In 1997, a team of research scientists demonstrated that mercury vapor inhalation by animals produced a molecular lesion in brain protein metabolism which was similar to a lesion seen in 80 percent of Alzheimer diseased brains.

Recently completed experiments by scientists at the University of Calgary’s faculty of medicine now reveal with direct visual evidence from brain nuron tissue cultures how mercury ions actually alter the cell membrane structure of developing neurons.
To better understand mercury’s effect on the brain, let us first illustrate what brain neurons look like an how they grow. In this animation we see three brain neurons growing in a tissue culture, each with a central cell body and numerous nurite processes. At the end of the end each nurite is a growth cone where structural proteins are assembled to form the cell membrane. Two principal proteins involved in growth cone function are actin (phonetic), which is responsible for the pulsating motion seen here, and tubulon (phonetic), a major structural component of the nurite membrane. During normal cell growth, tubulin molecules link together end to end to form micro tubules, which surround neuro fibroles (phonetic), another structural protein component of the neuronal axon (phonetic).

Shown here is the nurite of the live neuron isolated from snail brain tissue, displaying linear growth due to growth cone activity. It is important to note that growth cones in all animal species, ranging from snails to humans, have identical structural and behavioral characteristics and use proteins of virtually identical composition.

In this experiment, neurons also isolated from snail brain tissue were grown in culture for several days. After which, very low concentrations of mercury were added to the culture medium for 20 minutes. Over the next 30 minutes, the nurite membrane underwent rapid degeneration, leaving behind a denuded neurofibrole seen here. In contrast other heavy metals added to this same concentration, such as aluminum, lead, cadmium and manganese, did not produce this effect.

To understand how mercury causes this degeneration, let us return to our illustration. As mentioned, (technical difficulty) during normal cell growth to form the microtubules which support the nurite structure. When mercury ions are introduced into the culture medium, they infiltrate the cell and bind themselves to newly synthesized tubulin molecules.

More specifically, the mercury ions attach themselves to the binding site reserved for guanicine (phonetic) tryphosphate (phonetic), or GTP, on the beta subunit of the affected tubulin molecules. Since bound GTP normally provides the energy which allows tubulin molecules to attach to one another, mercury ions bound to these sites prevent tubulin proteins from linking together. Consequently, the nurites microtubules begin to dissasemble into free molecules leaving the nurite stripped of its supporting structure. Ultimately, both the developing nurite and its growth cone collapse, and some denuded neurofibroles form aggregates, or tangles, as depicted here. Shown here is a nurite growth stain specifically for tubulin and actin before and after mercury exposure. Note that the mercury has caused disintegration of tubulin microtubule structure.

These new findings reveal important visual evidence as to how mercury causes neurodegeneration. More importantly, this study provides the first direct evidence that low-level mercury exposure is indeed a precipitating factor that can initiate this neurodegenerative process within the brain.