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Re: DFRAI post# 381492

Friday, 11/04/2022 5:26:37 PM

Friday, November 04, 2022 5:26:37 PM

Post# of 463866
Interesting article and a bit over my head but my take away from the article is that the way to solve AD is by restoring upstream neuronal and cellular homeostasis!

It cites Paul Aisen, "Indeed, compounds (e.g., bapineuzumab, solanezumab, and gantenerumab) used in clinical trials to either reduce Aß42 production (e.g., ClinicalTrials.gov identifiers: NCT00470418, NCT01303744, NCT01421056, and NCT00606164) or prevent Aß aggregation (e.g., NCT00568776 and NCT00934050) have been unsuccessful in slowing down or preventing the pathophysiology of AD (Aisen et al., 2011; Mehta et al., 2017)

Additionally, we've wasted so many years down the amyloid theory rabbit hole keeping our blinders on to other areas for research. What a shame. "Failure in AD drug development so far might be related to... lack of drive to explore other pathological targets."

"Although some molecules have not yet been tested in AD models, we believe their proven MERCS (mitochondria–endoplasmic reticulum contact site) components have the potential to restore neuronal homeostasis."

Thanks for posting this. We're on the right path.

From Anavex
ANAVEX®2-73 activates the sigma-1 receptor (SIGMAR1). Data suggests that activation of SIGMAR1 results in the restoration of complete housekeeping function within the body and is pivotal to restoring neural cell homeostasis and promoting neuroplasticity.

ANAVEX®2-73 is an orally available drug candidate that restores cellular homeostasis by targeting sigma-1 and muscarinic receptors. Preclinical studies demonstrated its potential to halt and/or reverse the course of Alzheimer’s disease.
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