InvestorsHub Logo
Followers 164
Posts 19781
Boards Moderated 2
Alias Born 12/09/2004

Re: XenaLives post# 118097

Thursday, 08/31/2017 4:33:04 PM

Thursday, August 31, 2017 4:33:04 PM

Post# of 462249
It is narrower than "cellular homeostasis". The putative MOA is to improve the connection between the mitochondria and the endoplasmic reticulum in neurons.

In the case of neuronal dysfunction caused by the inefficient connection between the mitochondria and the ER then 2-73 is thought to improve that connection.

The disease path created by that inefficient connection appears to be caused by misfolded proteins manufactured in the ER due to lack of ATP normally sourced from the mitochondria. There may be other molecules generated by the mitochondria other than ATP that are not being adequately provided to the ER due to the faulty connection.

It is thought that this errant process is the beginning stages of a number of CNS diseases. 2-73 is thought to improve the connection and prevent the misfolding of proteins in the ER. These proteins have many different jobs in the neurons.

The hope is that by improving the upstream connection in the disease process that homeostasis is reestablished in the neurons. The consequences of having the misfolded proteins no longer being created may be the stopping of disease process and hopefully allowing the CNS to recover from some of the damage caused by the presence of the misfolded proteins through the normal healing processes.

Much of this has yet to be proven in humans. There is good murine data to support these expectations. Expectations are not definitive proof.

Bottom line.... It is CNS neuron homeostasis.


He said all he had to say long before he quit talking.

Volume:
Day Range:
Bid:
Ask:
Last Trade Time:
Total Trades:
  • 1D
  • 1M
  • 3M
  • 6M
  • 1Y
  • 5Y
Recent AVXL News