RSSCanada confirms mad-cow case
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However,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;
Report ViolationNeurodegenerative diseases, including BSE, Alzheimer’s 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.
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"simultaneo us" action on the ruminant tissues.
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".
Comments about this abstract; as a proof concerning Mg-deficiency (and hepatopathy; see www.bse-expert.cz ), 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 recent „Canada experiments“ as another confirmation about the BSE ammonia- magnesium theory (hyperammonemia-proteinemia and hypomagnesemia) in the neurodegeneration;
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.
Sincerely,
Josef Hlasny, DVM, PhD, Czech Republic