I am not a doctor, or a scientist. I discovered Sava in September 2020, and began doing my initial research on AD, including the history of efforts by drug companies to develop a drug for AD. I made a list of every biotech working on CNS problems, which caused me to discover AVXL. At that time, Dr Missling had not described A2-73's MOA very well or convincingly to me.
Looking at what others said about the chemical similarity between A2-73 and simufilan, and prevailing views about the process of neurodegeneration which leads to tau tangles, my initial thoughts were that A2-73 works similarly to simuflan by protecting neuron microtubules from the ravages of tau phosphorylation, thereby achieving similar results to SAVA.
After more review of the problem how stopping injury to neurons could potentially reverse AD symptoms and result in regained cognition, rather than merely slowing cognitive decline, I decided there must be more to the MOA of both drugs. Largely from my research on SAVA and the developing views in Alzheimer's research about the role of neuroinflammation, I concluded that reduction of persistent inflammation which is an important part of how SAVA is achieving improve cognition, likely also plays a big role in what sr1 activation achieves.
I now think that sr1 activation has a salutary effect to protect neurons from phosphorylation, and to reduce persistent inflammation that also is an agent of oxidative stress in older people with cognitive decline.
But my examination of muscarine receptors established that there were five widely studied musculine receptors, three of which already were active in different drugs, and two of which were like the sr1 receptor, thought to be potentially helpful in CNS diseases. My understanding of chemistry is very limited, only what I can remember from high school and the little I have done in studies thereafter, but it appears to me that the muscarine receptors, based on binding affinities and other chemistries, may have a large role in the outcomes that A2-73 can achieve for some patients.
Like shava claims it's drug has a dual action, it appears to me that A2-73 produces multiple downstream actions that are important in preserving CNS health. I couldn't isolate the specifics better until I started reading about a well understood concept of autophagy the doctor Missling started relying on as his moa A2-73.
The idea that sr1 causes autophagy and performs a "housekeeping function"seems to me to be an oversimplification but one that is understandable in concept. The introduction of the idea of cellular homeostasis into my understanding of A2-73 turned my thinking towards the possibility that A2-73 had multiple protective effects for the cell. Research on the translocation of The chaperone protein and the developing information offered by Dr missling turned my thinking towards the potential of natural evolved protective mechanisms created by evolution that A2-73 taps into by "activation" of SR1.
That started me looking at agonist, ligands and the chemistry of activation of sr1. This brought attention and focus on A3-71 which I'm understanding to be the result of an ongoing project at AVXL to find other ways to activate sr1 and potentially achieve different beneficial outcomes for CNS patients.
Looking at other companies that activate sr1, I discovered ASXM, a company that also activates sr1 with its ax-05' a drug currently being evaluated by the FDA for approval for the indication of drug resistant dementia. They have very good efficacy data, and to me this provides helpful confirmation that activation of sr1 is a route for potential drug development and FDA approval.
With the help of George, on this message board, I delved into the vast literature on sr1 and became increasingly more convinced that it has some extremely potent, and wide ranging powers to protect the cellular integrity when it comes under stress from a wide range of potential directions. Dr missling's corporate presentations drew my attention to the naturally evolved protections of the DNA code from mutation and errors, and I now think sr1 activation and/or muscarine receptor activation plays a role in protection of the DNA integrity.
Also, very helpful to one's understanding of sr1 are the ongoing trials, both animal and clinical, producing beneficial results in disparate indications that obviously do not have the same exact mechanism of action. The way that A2-73 is somehow achieving good topline results in, for example, retts, Parkinson's problems, and AD leads to the inevitable conclusion that there really are naturally evolved protective mechanisms for the brain and the CNS not widely understood previously, that sr1 triggers.
When you put it all together, it appears possible that AVXL can offer a drug that will be helpful to some extent yet uncertain in several CNS maladies. I called it a vector Force for improved health, as I see it and stabilizing the cell from many different negative mechanisms that harm it. My reading on how Alzheimer's occurs has led me to believe it is the product of a large number of different causes and problems of aging.
So I use a simplistic math model of bad forces and good ones affecting the brain in CNS indications, in a battle that always ends in death, with A2-73 as a superhero producing powerful vector forces that can prolong health but not cure anything yet.
One day, maybe, when medicine is much stronger, sr1 activation can possibly be part ofan even greater prophylactic fight against aging.
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