Tuesday, October 05, 2021 8:50:18 PM
Another well-founded, solid-science murine (lab rodent) study/confirmation of blarcamesine yielding quite remarkable results against a central nervous system (CNS) disease; in this case a murine model of fragile X syndrome.
Lots of very positive results in the study, but all summed in this statement: “When all 4 mouse groups were contrasted, chronic treatment with blarcamesine significantly reduced the behavior in Fmr1 KO2 mice to levels indistinguishable from those observed in vehicle-treated WT [wild-type, normally functioning] mice (Fig. 1a).”
Skim through the paper; notice the microscopic p-values. Everything stat-sig. Results real; not by chance.
Simply, the mice with fragile X syndrome, when treated with blarcamesine, were able then to behave in ways indistinguishable from normal, healthy mice. That’s what a “cure” is.
Now, of course, many will discount this study. Mice aren’t men (or children, with fragile X syndrome), it will be contended. No, mice aren’t people. But their neurons function (or get diseased) in almost exactly the same way as in humans. The biochemical pathways and processes of neuron and nerve functions are nearly identical. Murine sigma-1 receptor proteins accept blarcamesine as an activating ligand in exactly the same way, with the same results, as those in human neurons.
Those who wish to dismiss or hold in abeyance this study, pending a larger, more comprehensive clinical study in humans, are welcome to hold to that position. I doubt, however, that would be the position of knowledgeable parents of children with fragile X. It certainly is not the position of Dr. Hagerman, a world-class expert in fragile X syndrome; after she’s learned of the biology of blarcamesine.
Were I a betting man (I’m not), I’d lay on the table a few dozen of my AVXL shares, betting them against anyone else’s bet that blarcamesine will prove ineffective as a treatment for fragile X syndrome in a proper, full-scale human clinical trial.
The clinical results, forthcoming, for Rett syndrome, will firmly establish blarcamesine as a safe and very effective treatment for that rare genetic CNS disease. Next, of course, will be positive results from the Parkinson’s disease dementia study, to conclude sometime next year. An Anavex win, there, too. Then will be the results of the big blarcamesine against Alzheimer’s study. It will seal the notion that blarcamesine fixes a diversity of CNS diseases; diseases for which no other drugs work with any equivalent efficacy.
Now, based on this murine study, and lots of other CNS data, in both murines and humans, let’s not be surprised when the fragile X syndrome organization supports and establishes a final, full-scale human trial of blarcamesine against fragile-X. But a matter of time.
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