Why Blarcamesine Might Be Working Against P. gingivalis $CRTX $AVXL $ANVS $SAVA

This Blog Is Only For Educational Purposes. Do Not Trade On This Blog Alone. Do Your Due Deligence or Consult Professional.

I have been directed by the author to an article about $CRTX and the evidence that Alzheimer’s might be caused by virulence of the bacterium P. gingivalis. The bacterium can hitch a ride from the mouth on cells of the immune systen and enter the brain through the Brain Blood Barrier. Then it slowely makes its way infecting neuron after neuron. The article documents in exquisitely detailed manner many aspects of this infection. Indeed, the evidence is compelling.

Nevertheless, drugs like $AVXL’s Blaracamesine do make difference in the progress of the disease. If truly the disease had been caused by germ infection then how a drug which was an agonist to SIGMAR1 receptors and in very general terms worked by restoring autophagy, homeostasis and doing some work around chromatin remodeling seems also to work on a bacterial infection?

The answer is that the P. gingivalis is interacting with humans in very insidious and complex manner. It takes about 25-30 years from infection to the manifestation for the infection. But what is most interesting that the action of gingipains, that is the proteases which the bacteruim produces cut proteins into smaller fragments and feed on them. The P. gingivalis bacterium is not an ordinary prasite, it downregulates genes and upregulates gene on its feeding preference. The article beautifully documents this. Let me quote the author Gordon Gecko was a Commie (SeekingAlpha privet blog): link: https://seekingalpha.com/instablog/20791881-gordon-gecko-was-a-commie/5613017-cortexyme-s-gingipain-theory-of-alzheimer-s-disease-pathogenesis

• Pg / gingipains display an astonishing ability to toggle our genes in ways that benefit their survival. A recent paper[xxiii] shows that of 15K genes studied, Pg upregulates 942 genes, and downregulates 1247 genes. Interestingly, this paper documents how Pg tends to upregulate the genes that code for proteins containing arginine or lysine, which are the sources of food and nutrition that gingipains can chomp on. The reverse is also true—Pg downregulates that genes that code for proteins lacking arg or lys that gingipains cannot attack. These upregulated and downregulated genes tend to be concentrated in the hippocampus; it is often observed that hippocampal volume shrinks in AD patients. The evidence seems to show that gingipains are especially active in this brain region, which would seem to explain why hippocampal shrinkage is so commonly seen in AD patients MRIs.

It is richly researched article. My admiration goes to the author for his deep knowledge. Had the alteration to chromatine be done by the bacterium would the suspected or rather documented chromatin remodeling by Blarcamesine would change this? We only have circumstantial evidence for the involvement of SIGMAR1 agonists with chromatin remodeling throught the results in the phase2a, the work on SIGMAR1 agonist cocaine, and its therapeutice effect on sufferes of Rett Syndrome. In previous post I gave link to paper documenting in research which concluded that cocaine block transcription of and the enzyme which broke down dopanine – feel good neurotransmitter.

Other papers (can be found on $CRTX website) described disruptions in autophagy and accumulation of proteins in the cytoplasm. Here again, the research on Blarcamesine show that it can clear the path to cellular health.

It might also be that the drugs from $CRTX, $ANVS, $SAVA and last but not least $AVXL can create a potent cocktail to cure Alzheimer’s once and for all. It seems that $CRTX drug binds to its proteases, $ANVS works in some unexpalined way still or cuts inflammation, $SAVA addresses the Filamen A and the cytoplasmic skeleton damage, and $AVXL reverses the chromatin remodeling done by the bacterium and also removes the barterium with its metabolism products.

I am not a scientist. This is both an advantage and a curse, since I barely have any detailed knowledge but I can see what escapes those who are entangled in mass of details, someties even contradictory. I am free to explore possibilities as I am unencumbered by amassed knowledge on any particular paradigm. This is both a strength and a weakness just the same applies to the mirror image of this dilema.

Please, take this post with grain of salt. Nevertheless, Dr. Missling himself has said that it is entirely possible that there will be a few drugs addressing Alzheimer’s as it is a very complex disease. I think that the results from the clinical trials shall prove Dr. Missling right.