JERUSALEM, Israel-Ruth Gabizon, MD, has reportedly discovered a marker that others have been hunting for more than 20 years. The Israeli scientist, from Hadassah University Hospital in Jerusalem, has found a protein molecule in the urine of people and animals infected with Creutzfeldt-Jakob disease (CJD).
This discovery could lead to test for animals and people thought to be ill from the variant form of CJD, more commonly known as Mad Cow disease.
However, controversy is brewing about the test before it has even been developed. Researchers have not determined the incubation period of vCJD and there have been reports that certain genetic conditions could speed up this time period for certain people. Some estimates have been as long as 30 years between the time of infection and death. This could keep people from wanting to take the test, fearing lack of medical insurance or other health related consequences from testing positive.
Gabizon's study, which was published electronically on June 21 and will be published in the Journal of Biological Chemistry in September, has pushed researchers to once again examine urine for clues to this disease.
Neil Cashman, MD, a professor of neurology at the University of Toronto said scientists have been looking for infectious prions in urine for more than 20 years unsuccessfully. Many of them moved on to look for these proteins in blood instead, but they are not flocking back to urine research in droves.
The financial impact of a test to identify sick animals and people would be massive. The European Union now requires all animals that are more than 30 months old be tested for mad cow before being slaughtered. The test requires a brain biopsy and can be expensive.
The American Red Cross has also recently instated new blood restrictions to prevent the disease from entering the American blood supply. Donors who have visited or lived in Europe are now subject to closer scrutiny.
The difficulty keeping this discovery from happening earlier lies in the quantity of the prions researchers are looking for. These proteins are present in the blood and urine in such small amounts that present technology cannot find them-or couldn't find them until Gabizon separated the different elements of urine during her experiment. She theorized that if the proteins that cause both forms of CJD were present in the lymph nodes, they would end up in the bloodstream. From there, they would be passed into the kidneys to be filtered out of the body because human enzymes cannot break down abnormal proteins.
From the kidneys, Gabizon figured the proteins would be so small that they would pass through into the urine. This is where the process becomes complicated. The kidney's have urea, a preserving substance that keeps proteins from folding. To keep the deviant protein from being altered by urea, they had to separate the two.
The urine of infected hamsters, humans, and cattle was placed into a machine that separates urea and lets the proteins return to their original shapes. These proteins are then exposed to the natural enzymes found in the kidneys.
In Gabizon's experiment, one protein consistently didn't break down in the urine of infected patients.
Tests have shown the protein is somewhat infectious. Animals injected with the protein did not develop the disease after 300 days of observation, but are still being monitored.
The people who were studied in Gabizon's experiment had the genetic version of CJD. They were not infected from the variant form, which is caused from eating tainted meat. More than 100 people have died in Europe from this variant.
Gabizon's work is being reviewed and labs around the world are trying to recreate her results. More information about the urine marker is expected within a month.
Information from www.nytimes.com</>