That Little Cell Stress That Does It….Or Right Chaperone Protein For Right Misfolded Protein In Alzheimer’s and Parkinson’s. $AVXL Blarcamesine.

Do not trade this blog as 4 billion years of evolution is against me and possibly even God laughs at it, He has a great sense of humor!

More Research Papers Pointing to SIGMAR1 Agonists As Possible Drugs For Alzheimer’s and Parkinson’s

Please, read this article on the cell stress and its effect of misfolded protein in cells.

Link: https://medicalxpress.com/news/2022-05-stressed-cells-clues-build-up-toxic.html

In some sense this article could not be possible without the imaging technology which allows to visualize the  transition from misfolded proteins to properly folded in the living cells. Tools like this advance the the biology of cell. Without them the progress in understanding the cell processes would not have been possible.

What are the Heat Shock Proteins? For those seasoned readers I will post a link to Wikipedia page, link: https://en.wikipedia.org/wiki/Heat_shock_protein

To make a long story short, we have been given the narrative on SIGMAR1 agonist as compounds able to release from Mitochondria Associated Membranes (MAM) all kinds of proteins stored there. Most of them are related to response to cellular stress or are chaperone proteins involved in proper folding of other proteins. This general description fits the same for Heat Shock Proteins. Some of them are related to response to elevated temperature like those involved in infections (fever) or overheating, as the name suggests and the history of discovery implies. Some are related to embryonic development where they serve as chaperons for proper folding of overabundance of synthesized protein.

In short, diseases like Alzheimer’s or Parkinson’s are characterized by build up of misfolded protein, that cause damage to the neurons. These misfolded proteins should have been either refolded properly or scraped altogether, broken down to amino-acids in lysosome instead they aggregate in the cells. The scientists reasoned that stressing the cell could result in further aggregation of misfolded proteins. Yet, the opposite has taken place. Mildly stressed cells have responded by refolding the aggregated proteins and return to health.

It has been observed that frequent sauna users have lower incidence of dementia.

Dr Avezov speculates that this might explain one of the more unusual observations within the dementia research. “There have been some studies recently of people in Scandinavian countries who regularly use saunas, suggesting that they may be at lower risk of developing dementia. One possible explanation for this is that this mild stress triggers a higher activity of HSP [Heat shock Protein], helping correct tangled proteins.”

Blarcamesine Works Better At Preventing Dementia Than Even Sauna….?

Heat Shock Proteins are varied group of proteins. In this article it is suggested that one particular protein from the entire class is involved in this effect. Nevertheless, the mild stress migth trigger a release of one particular protein in torrent of other proteins. As usual, the article describes a paradox which is no surprise for investors in Anavex Life Scienses. The SIGMAR1 platform drugs are to release indiscriminately content of MAM’s into cytoplasm causing similar effect to stressing the cell. If this starts soon enough, as the new murine model of Blarcamesine shows even the onset of the disease (Alzheimer’s or Parkinson’s) is prevented. On the other hand, the disease process might be so advanced that the natural process could be to little avail.

The new murine model dosed mice with Blarcamesine before the introduction of amyloid plaque into their brains which should cause symptoms similar to Alzheimer’s. Upon the injection of amyloid plaque the mice did not developed symptoms of Alzheimer’s. In a similar fashion to the frequent sauna users the mice did not developed dementia. I hope that the heading’s veracity will hold in further trials.

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