Science is Broken
     

Gary Novak

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Description of Prion Activity
 

Supposedly, these diseases are spread by proteins bumping into each other. When do proteins not bump into each other? Why is a particular bump needed to start the processes? There is no biochemical mechanism for distinguishing one type of bump from another.

Here's a description of how the supposed prion disease works and the related science. All cells have membranes for holding enzymes in place and creating chambers. Various molecules must pass through the membranes. Small molecules sometimes diffuse through. Complex molecules are usually carried across the membrane by transport proteins.

protein

Proteins are designed for specific recognition. Transport proteins will recognize and attach to a specific molecule. They then move that molecule across the membrane and leave it on the other side. To do that, transport proteins have two configurations—one configuration for each side of the membrane. They flip back and forth hundreds of times per second changing configurations and moving a substance across the membrane.

The claim is that one of the configurations of a brain transport protein is the cause of Mad Cow Disease. Several years ago, some Britians got Mad Cow Disease by eating meat from cows which had the disease. If a brain transport protein were the cause, here's what would have to happen:

The brain protein had to get into the meat. An impossibility. Brain proteins cannot get out of the brain. Then the digestive system had to ignore the brain protein while digesting the rest of the meat. Then the brain protein had to circulate through the blood stream of the victim without the immune system removing it. Foreign proteins are very easy to recognize by white blood cells which remove foreign matter from the blood.

Then the foreign protein had to go across the blood-brain barrier. Brains do not have blood in them, they have a different fluid, and only a few nutrients and small molecules can get into the brain from the blood. But a foreign protein somehow gets across. Then it bumps into a normal transport protein in the brain and causes it to change to one of its configurations, which it normally does hundreds of times a second. The result is Mad Cow Disease.

Omitted in the claimed mechanism is how the lesions form. Plaques form in the brains of diseased animals. The plaques consist of aggregates of a brain transport protein which were produced in excessive amount. The disease organism causes plaques to form in the brain by causing an over-production of the transport protein.

To produce too many proteins requires the protein synthesizing machinery to over-produce. This would require too many copies of the genetic material to be produced and too much ribosomal activity. The real cause of the disease turns this machinery on to create plaques. How does a brain transport protein cause this machinery to over-produce? No explanation is given. The only explanation is that existing transport proteins are contacted causing them to form a bad configuration.

In other words, almost every element of biology is contradicted in claiming a brain transport protein causes diseases related to Mad Cow Disease, and none of the complexities are explained.

Stanley Prusiner did about a dozen junk science studies to show that the prion protein is the causative agent for such diseases, and he got a Nobel Prize for it. The bureaucrats produce dozens of such studies each year to confirm Prusiners conclusions.

Prion Main Page

 

 

           
 
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