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Re: Fireman02360 post# 295462

Tuesday, 02/02/2021 8:22:57 PM

Tuesday, February 02, 2021 8:22:57 PM

Post# of 463611
Probably not, but....

...can 2-73 fix the FLNA/ scaffolding protein after its been altered?

Probably not. Once the altered (misfolded?) FLNA proteins are in place, and malfunctioning, they are likely to remain there and continue to disrupt normal neuron chemistries. That would be the case, certainly, in the absence of blarcamesine therapy.

But the intelligent question arises, after the altered FLNA proteins are in place and causing Alzheimer's symptoms, could blarcamesine either a) restore the normal structure and functions of the in-place, altered FLNA proteins, or b) simply replace or displace them with new, fully functional proteins?

I doubt that option a) would work. Blarcamesine does its work in the sigma-1 protein, not directly on any downstream proteins (of which FLNA is apparently one). I see no mechanism by which blarcamesine could re-configure, to a normalized architecture (and function) the altered FLNA proteins.

But, rather certainly, with the production of new, normal FLNAs after the blarcamesine therapy has begun, those new, normally functional FLNA proteins will displace, replace the older, malfunctioning ones. The biochemistry of the neuron will almost surely favor the new, fully functioning FLNA proteins.
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