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Study Looks At Mitochondria In Genetic Model Of Parkinson’s
The fabled energy machines of the human cell, Mitochondria, have been for long regarded as ancient organisms which evolved from symbiotic organism into indispensable organels of human cells (animal and plant cells). The vestige of this process is the fact that Mitochondria posses their own DNA, transferable from human generation to generation through the maternal germ line. Mitochondria behave like they are their own organism and they divide and merge. Researchers from California NanoSystems Institute identified two proteins connected with Mitochodria’s ability to fission or divide (multiply?). Also Mitochondrial can merge. You can read all about it at this post  https://medicalxpress.com/news/2022-03-protein-awry-parkinson-disease.html. This in itself might be interesting for people who invest in Anavex Life Sciences as Blarcamesine or know otherwise as Anavex2-73 as its MOA has been long connected with Mitochondrial health.
There has been circulated hypothesis that agonists of SIGMAR1 receptors, one of them is Blarcamesine, cause the release of the proteins which are transcribed from the genetic material in the nucleaus and are translated form messange RNA on the surface of Endoplasiic Reticulum. Mitochondria Associated Membranes (MAM), located on Endoplasmic Reticulum, are thought to be the final stages of this process where the energy from Mitochodria is used to fold the protein into the spatial configurations for proper function. The action taken by the agonist of SIGMAR1 release the proteins from the MAM into the cytoplasm and ultimately the intercellular matrix. It has been also observed that Blarcamesine improves the Mitochondrial health.
As scientists work toward finding a cure for Parkinson’s disease, one line of research that has emerged focuses on mitochondria, the structures within cells that make energy. The health of those structures is maintained through a quality control system that balances two opposite processes: fission—one mitochondrion splitting in two—and fusion—two becoming one. 
The human proteins CLUH and Drp1 are involved in the maintenance of Mitochodrial health by keeping the balance between propensity to fission (divide) and fusion (combine together). Let’s see a quote from the source.
The study, published today in Nature Communications, found that a protein in humans called CLUH (pronounced “clue-H”) acts to attract Drp1 to mitochondria and trigger fission. In experiments with fruit flies that were genetically engineered with an analog for Parkinson’s disease, the team showed that damage from the disease could be reversed by increasing the amount of a protein that scientists call “clueless,” which is the fruit fly equivalent of CLUH. 
So right now we have a signaling pathway or cascade of two proteins and the complexity of the disease has been reduced to the problems with fission of Mitochondria resulting from the deficiency of CLUH and Drp1 proteins.
When there’s a problem with fission, that system is thrown out of balance. The consequences can include neurodegenerative diseases, such as Parkinson’s disease, and other serious conditions. 
The researchers are optimistic that they can focus and the minute detail of these two protein interactions with Mitochondria and the problems of fission/fusion to design a drug to restore balance (induce fission) to cure, in their minds, not only Parkinson’s.
“With a critically important pathway such as Drp1, there might be multiple proteins we could use to intervene and ultimately control Parkinson’s disease,” said Dr. Ming Guo, the corresponding author of the study and a professor of neurology and of molecular and medical pharmacology at the David Geffen School of Medicine at UCLA. “When we modified clueless in flies, symptoms analogous to Parkinson’s disease improved substantially.” 
If this would not be enough……
Guo’s research focuses on neurodegenerative conditions, but disruptions in the fission of mitochondria are behind a host of other ailments, including cancer, diabetes and heart disease, as well as some developmental defects that lead to infants’ death.
Don’t we already have a drug with at least partial capabilities like the ones on which Dr. Ming Gao is ready to focus on developing? I have once called Blarcamesine the Swiss Army knife of a drug. The MAM contain many varied protein and some belive they are retained there for the moment the cell would be under stress. Some of these protein might address the Mitochondrial health, others might work on other signaling pathways. If indeed Parkinson’s etiology involves Mitochondrial health and Blarcamesine addresses this fault in the cellular health then we have this drug just to be approved. The pattern of Blarcamesine results supports this assertion. For time being, it is Rett Syndrome, Alzheimer’s and Parkinson’s. What if the latter quote implies that Blarcamesine can be an actual life extension drug? The evidence and circumstantial evidence, also the narrative from the company CEO point in this direction. This is just another piece of info supporting amazin vesatility of Blarcamesine
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