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rogue proteins

Posted: Sat Dec 20, 2014 1:33 pm
by 1eye

Re: rogue proteins

Posted: Sun Dec 21, 2014 1:03 pm
by 1eye
This is from the last part of the study this article is about. (my emphasis)
Our study shows for the time that protein aggregates detected by anti-oligomer specific antibodies are associated with MS. The data generated so far does not allow to reach a substantive conclusion in relation to the involvement of these proteins aggregates in MS pathogenesis. Protein aggregation associated with MS has been described previously in a rodent model of MS (16). Dasgupta and colleagues have demonstrated increased protein aggregation in the spinal cord of mice with experimental autoimmune encephalomyelitis (EAE). In their study, they argue that accumulation of misfolded proteins is caused by increased rate of protein oxidation and reduced proteasome degradation, both seen in MS (17) and EAE (18, 19).

In conclusion, for the first time, we demonstrate the presence of soluble oligomers, normally associated with PMDs, in MS tissues and CSF. Although the pathogenic relevance of these MS associated soluble oligomers to disease process remains to be investigated, this study sets the ground for further investigating this relationship. This study proposes a novel alternative in understanding the pathogenesis of MS.
PMD=Protein Misfolding Diseases. So it seems some people think that oxidation of proteins is causing this misfolding, which may at least be a marker of of "MS", if not a cause. This may relate to the low oxygen consumption in the brains if those with "MS", which is suspected to be caused by excessive nitric oxide, interfering with mitochondrial processes necessary for oxygen and glucose use. This, in turn, may come from inducible nitric oxide synthase (iNOS) created by immune cells, which can get where they don't belong when the blood-brain-barrier leaks. Can you see where brains are in double-jeopardy?

As an aside, RF can cause BBB leakage:


From Blood‐brain barrier permeability in rats exposed to electromagnetic fields used in wireless communication
The frequency of pathological rats is significantly increased (p < 0.0001) from 62/372 (ratio: 0.17 ± 0.02) for control rats to 244/630 (ratio: 0.39 ± 0.03) in all exposed rats. Grouping the exposed animals according to the level of specific absorbed energy (J/kg) give significant difference in all levels above 1.5 J/kg. The exposure was 915 MHz microwaves either pulse modulated (PW) at 217 Hz with 0.57 ms pulse width, at 50 Hz with 6.6 ms pulse width or continuous wave (CW). The frequency of pathological rats (0.17) among controls in the various groups is not significantly different. The frequency of pathological rats was 170/481 (0.35 ± 0.03) among rats exposed to pulse modulated (PW) and 74/149 (0.50 ±0.07) among rats exposed to continuous wave exposure (CW). These results are both highly significantly different to their corresponding controls (p <0.0001) and the frequency of pathological rats after exposure to pulsed radiation (PW) is significantly less (p < 0.002) than after exposure to continuous radiation (CW).