Changes in urine could lead to BSE test for live animals

September 5, 2008

Researchers have demonstrated that protein levels in urine samples can indicate both the presence and progress of Bovine Spongiform Encephalopathy (BSE) disease in cattle. Publishing their findings in BioMed Central's open access journal Proteome Science, the scientists hope that their discovery might lead to the development of a urine-based test that could prevent the precautionary slaughter of many animals as now occurs when the disease is detected.

The discovery of a new human variant of Creutzfeldt-Jakob Disease (vCJD), thought to be transmitted to humans via BSE-infected products, has resulted in many countries instituting extensive BSE testing programs for older animals. Diagnostic testing currently involves the detection of a misfolded "infectious" protein, or prion, in post-mortem brain tissue.

BSE has caused significant changes in the way beef products are produced and traded. If a simple and accurate urine test can be developed from this new knowledge, it could be performed on live animals and therefore may provide an alternative to current BSE surveillance procedures. It could also allow for the assessment of the health of breeding stock where post-mortem testing is not an option.

"We are hopeful that the knowledge that we've gained from this study will eventually lead to a live test," says Dr. David Knox, a researcher at the Public Health Agency of Canada's National Microbiology Laboratory in Winnipeg. "It may be possible to develop similar tests for other species as well, including humans with Creutzfeldt Jakob disease (CJD). A urine test for CJD could assist doctors to narrow down potential diagnoses for people with dementia".

Knox led a team of researchers who have demonstrated that the "protein profile" of cattle urine samples can indicate the presence of a BSE infection as well as how far the disease has advanced. The scientists analysed the proteins in urine samples taken from four infected and four healthy cows of the same age over the course of the disease. The proteins from the healthy and infected samples were compared using a technique called two-dimensional differential-gel electrophoresis (2-D DIGETM)

In these preliminary results a single protein was able to distinguish between those infected and control animals. In addition, the relative abundance of a set of proteins could accurately determine how far the disease had advanced.

"Our work shows that it is possible to identify biomarkers in urine that could be useful in the diagnosis and monitoring of disease progression in BSE and related transmissible spongiform encephalopathies," says Knox.

Source: BioMed Central

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not rated yet Sep 06, 2008
According to my opinion mad cow disease (BSE) is not an infectious disease. See my recent presentation at 29th World Veterinary Congress in Vancouver ( ; Neurodegenerative Diseases and Schizophrenia as a Hyper or Hypofunction of the NMDA Receptors. There is the abstract about this article;

Neurodegenerative diseases, including BSE, Alzheimer%u2019s disease etc. are caused by different mechanisms but may share a final common pathway to neuronal injury due to the overstimulation of glutamate receptors, especially of the N-methyl-D -aspartate (NMDA) receptor subtype. It is generally accepted that the influx of Ca2 as a result of excessive activation of the NMDA receptor underlies the toxic actions of glutamate in many systems. Also, ammonia intoxication leads to excessive activation of NMDA receptors in brain. On the other hand, Mg2 competes with Ca2 at voltage- gated calcium channels both intracellularly and on the cell surface membrane. So, Mg2 can protect against NMDA- induced neurodegeneration and Ca2 deficiency can be important about "NMDA hypofunction" in schizophrenia. In addition there can be another example about hypoglutamatergic condition; cannabinoids are known to inhibit Ca2 channels- glutamate release in schizophrenia, and to inhibit progression of certain neurodegenerative diseases.
There are no scientific references to date in which high intake of crude protein (and potassium) high enough to lead to a state of hyperammonemia (and hypomagnesemia) during the incubation period of the BSE. Therefore there is the first idea of this review; to show the hyperammonemia plus hypomagnesemia"simultaneous" action on the ruminant tissues. So the various clinical symptoms can be observed because the nervous system controlling both voluntary and unvoluntary muscles is affected (Mg and Ca disturbances). If the BSE is involved; a longer- chronic action of corresponding biochemical changes in the blood (CSF) is necessary, to rise irreversible neurodegenerative changes.
Recently was found that elevated manganese in blood was associated with "prion infection" in ruminants. These findings about "manganese theory" act in concert with this "BSE ammonia- magnesium theory". So I will perform some interpretations about this connection and some details will be presented to the Congress, and also second idea of this review; to show that cannabis use can be a proof about the link between the NMDA receptor hyperfunction (neurodegeneration) and hypofunction (schizophrenia).
Comments about this abstract; as a proof concerning Mg-deficiency (and hepatopathy; see , according to the alternative BSE ammonia- magnesium theory;
1. In biological systems, only Mn2 is readily capable of replacing Mg2 , and only in a limited set of circumstances. The body can replace Mn with Mg with similar efficiency in Mn-activated proteins (1990). Similarly, Mn can occupy Mg allosteric sites in Mg-activated proteins, such as the sarcoplasmic reticulum Ca- ATPase (1981). It was found (1999) that feeding rats a diet deficient in Mg; decreased urinary - fecal Mn excretion and greater Mn retention in skeletal muscle, heart and kidney (except the liver and trabecular bone) in Mg-deficient rats was observed.
2. Other cause about Mn deposits in tissues is liver disease. People with chronic liver disease have neurological pathology and behavioral signs of Mn neurotoxicity, probably because elimination of Mn in bile is impaired (1994- 1996). This impairment results in higher circulating concentrations of Mn, which then has access to the brain via transferrin. It was reported that whole blood Mn concentrations significantly increased in patients with chronic liver disease.
Comments about two recent (Canada,2008) experiments as another confirmation about the BSE ammonia- magnesium theory (hyperammonemia-proteinemia and hypomagnesemia) in the neurodegeneration;
1. Normal prion protein (PrPc) might function to block some NMDA receptors and thereby prevent overexcitement and death of neurons. Recently researchers at the University of Calgary (April, 2008) found; when the nerve cells received the messenger glutamate, they went into hyperactive mode, however, when also Mg was removed from the cells, the brain cells went into seizure mode.
2. Scientists from the University of Manitoba found that changed levels of a set of proteins in cattle urine indicates the presence of BSE with 100 per cent accuracy in a small sample set. So the discovery of elevated protein levels in the urine of some cattle with mad cow disease raises the possibility that live animals could be screened.
not rated yet Feb 04, 2009
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