Is There More than Just Alzheimer’s, Parkinson’s and Rett Syndrome in Blarcamesine Bag of Tricks? $AVXL

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See press release from Anavex Life Sciences.

Heart has its own little nervous system which in part is independent from the brain. Blarcamsine as SIGMAR1 agonist does its work as far as we know primarily in the nervous cells. Yet, the SIGMAR1 receptors are expressed in different organs too. I was trying to provide a detailed list but unfortunately it is much harder task than a quick search. Leaving this aside, is there general health advantage to Blarcamsine besides CNS health? We can speculate on this due to the nature of Blarcamesine action on SIGMAR1 receptors as detailed in this post .

To just shortly explain, agonists of SIGMAR1 cause the release of large number of health improving signaling molecures. Is there already evidence that Blarcamesine can alter the general health of those receiving it? I looked at certain data from reference study

I created an illustration and published it two weeks ago without extensive explanation. I am attempting to provide some logic under which I constructed the graph. Let’s see the graph.

  • There are two lines. One (dashed) is for probable Alzheimer’s patients numbers remaing in the reference study over a period of 7 years. The other is the controlled group consiting in 50% of healthy spouses or volunteers reporting every year for check up.
  • Both groups are very similar in make up, the only difference being the probable Alzheimer’s diagnosis. For the Alzheimer’s cohort the reason for no showing up can be deterioratiom due to demantia, death, or general health deterioration. For the controls cohort it can be the same, save the dementia.
  • The number of no-shows is expresed in percent of starting cohort group population still reporting. 32 patients in Phase 2a study is consitent with the minimal sample of a general population. The reference study used about 300-400 participants to arrive at these plots.
  • The first year Phase 2a loses more patients than the reference study so arrow is red and pointing down.
  • The second year, the phase 2a numbers are comparing favorably with the precentages of participants staying with Alzheimer’s staying in the study so arrow points up and is green.
  • By third year the patients from the phase 2a study are in the Open Label Extension for two years. The procentage of popluation of Phase2a OLE still within the study seems to emulate the population of the healthy cohort in the reference study. Can we state that the morbidity due to Alzheimer’s has been removed from the Phase 2a participants?
  • We do not have data for the 4th year of the study.
  • We now reach the 5th year of the study. In the statement by Dr. Missling the number of patients within the study has been set between 10 and 21. With 10 patients we “remove morbidity due to Alzheimer’s”, but with more than 10 patients left with the study the implication is that the general health of the patients improved over the level of those participating in the healthy controls cohort of the reference study.
  • Caveat: The Phase 2a study has not been designed to answer this question. Neither, we know for sure the doses received by the patinets in the OLE extension.
  • A word of caution, this is a very creative way at looking at the data but the word “creative” has as on its other side the meaning of something unbecoming. This is just an excersize in free style data analysis. I could be close to the truth or can be way off, so please take it with grain of salt.


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