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The Nature Of Balrcamesine Mechanism Of Action.
The detractors of $AVXL always was list the closely unknown MOA. Most drugs are working in one point in some specific pathway. Their mechanism of action can be easly indentified by a single molecule they substitute for or interact with. The MOA for Blarcamesine is so vague and broad that it is presently thought to be involved with two basic and complex processes in celullar biology. These are transcription and translaton, or reading genes and folding the proteins synthesized from the reading. These two processes are so complex that at this moment we have just few glimpses into them. That is why the number of papers just uncovers the importance of these processes in the neurodegenerative and neurodevelopmental diseases, but they fail to bring to focus the inner workings of those processes as they just uncover interaction with few elements of the complex whole. We, for example, might know that certain genetic mutations are connected with Authism Spectrim Disorders but the exact disruptions to specific pathways has not been elucidated yet. It will take log time to assemble detailed knowledge of various interactions to pieces some basic theory of inner workings of transcription and translation as it is affected by SIGMAR1 receptors agonists. Meantime, we are just left with clues to their therapeutic action.
Another Clue To Complexity of ASD Lists Transcription and Translation As Culprits.
Please, read article at this link https://medicalxpress.com/news/2022-07-autism-related-mutations-inhibit-export-key.html
From this article one can gather that we are identifying the genetic causes of ASD but are less adept at having insight into inner workings of these mutations in the celullar biology or their corresponding pathways. Nevertheless, in one case the mutation in gene Usp15 might be causing error in the transcription in the protein chain resulting in misfolded protein interfering with the edondoplasmic reticulum ability to fold proteins. The name of the protein is Hevin. From the article it seems that Hevin is a protein involved in disruption of workings of the edoplasmic reticulum by agreggating in it. Whenever we hear about the MOA of Blarcamesine as SIGMAR1 agonist we hear of setting in motion processes either clearing bu;dup like this or preventing it altogether. There is growing body of knowledge connecting the ASD with particular aspect of celullar biology. Let me quote the autor of the article.
Given that several other autism-related mutations have also been shown to promote the accumulation of synaptic proteins in the endoplasmic reticulum, it is possible that the resulting impairment in neuronal function contributes to autism pathogenesis. Future studies may help reveal how the endoplasmic reticulum stress response affects neural circuits and brain homeostasis and clarify the link to autism development.
In general, Blarcamesine can be blanket treatment for many CNS neurodegenerative and neurdevelopment diseases, among them ASD, but that has to corroborated by clinical trial or at the least one can start with murine models. Here, once we start talking murine models, it behoves us to say that Blarcamesine never failed to translate the murine model to success in clnical trials so our expectations are high.
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