A new study, investigating how endoplasmic reticulum dysfunction can cause waste protein accumulations that cause Alzheimer’s symptoms, fits exactly the Anavex mechanism of action (MOA).
Previous studies have suggested that ERAD [ the mechanism by which cells get rid of proteins that are folded incorrectly in the ER ] contributes to many diseases where cells become overwhelmed by an irregular accumulation of proteins, including Alzheimer's," says Xu. "This study provides conclusive, mechanistic evidence that ERAD plays an important role in restraining Alzheimer's disease pathology. We now plan to search for compounds that enhance production of membralin or the rate of ERAD to test whether they ameliorate pathology and cognitive decline in models of Alzheimer's.
This matches perfectly with the ever-clearer Anavex MOA, where the Anavex molecule re-connects separated endoplasmic reticula with mitochondria. When this happens, the mitochondria can resume ATP production and easily pass the energy-supplying ATP molecules over into the endoplasmic reticula, where the energy is used for normal chemistry there. Among other chemical processes in the ER is the proper folding of enzyme proteins, and elimination of improperly folded ones.
All of that normal functionality was found in this study (as expected).
And, Anavex Life Science Corp could surely complete the researchers’ plan, “We now plan to search for compounds that enhance production of membralin or the rate of ERAD to test whether they ameliorate pathology and cognitive decline in models of Alzheimer's.”
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