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Re: Amatuer17 post# 406568

Friday, 03/10/2023 7:35:21 AM

Friday, March 10, 2023 7:35:21 AM

Post# of 470038
Blarcamesine and the new mitochondrial theory of Alzheimer's:

Blarcamesine and the new mitochondrial theory of Alzheimer's article from New Scientist.

Quoting from Mayomobile's sotcanalytics.com:

Anavex called out 65 specific genes which have had significant analysis conducted separately via the KEGG 2022 database. ... Notice ... the propensity for certain genes to be degraded in both [Parkinson's and Alzheimer's]. ... [T]he immediate top-level implications are readily available. Blarcamesine is re-enabling the function of these genes, which have significant roles in:

Genes implicated in the mitochondrial electron transport chain (all parts from beginning to end)

Genes responsible for maintaining the genes used for mitochondrial electron transport chain

Protein homeostasis by removing misfolded or damaged proteins, which could impair cellular functions, and by removing proteins whose functions are no longer required

Genes that cue the removal of misfolded or damaged proteins mentioned above

Transduction of components through the membrane of the mitochondria

Master regulation of mitochondrial energy output by balancing ATP production and thermogenesis

Processing amyloid beta proteins


In the quotation above, for brevity I've edited out some of the items in Mayomobile's list. I've left in the ones referencing mitochondria; and I left in the one about "Processing amyloid beta proteins," just to highlight that the amyloid plaque, which Big Pharma has myopically focused on as a "key driver of cognitive decline," is just one downstream effect of a fundamental dis-regulation or deterioration of cell function, which blarcamesine addresses and the amyloid-clearing monoclonal antibodies do not.

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