Replies to post #362160 on Anavex Life Sciences Corp (AVXL)

[tredenwater2]

Thanks falconner! Your continued solid posts are very valuable here, especially as e near the release of TLD. I get the feeling this board and stock will heat up and quick.

[plexrec]

"That’s exactly what blarcamesine facilitates:"--yikes--if true WHT---WTF---we do HT !!!!!

[toemind]

Wonderful find Falconer!
ToeMind

[abew4me]

Wow. This is huge. Thanks falconer!

Quote:
“Our results for the first time sources neuronal damage observed in Alzheimer’s disease to problems inside brain cells’ lysosomes where amyloid beta first appears,” says study lead investigator Ju-Hyun Lee, PhD.

“Previously, the working hypothesis mostly attributed the damage observed in Alzheimer’s disease to what came after amyloid buildup outside of brain cells, not before and from within neurons,” says Lee, a research assistant professor in the Department of Psychiatry and NYU Langone Health and research scientist at Nathan Kline.

“This new evidence changes our fundamental understanding of how Alzheimer’s disease progresses; it also explains why so many experimental therapies designed to remove amyloid plaques have failed to stop disease progression, because the brain cells are already crippled before the plaques fully form outside the cell,” says study senior investigator Ralph Nixon, MD, PhD.

“Our research suggests that future treatments should focus on reversing the lysosomal dysfunction and rebalancing acid levels inside the brain’s neurons,” says Nixon, a professor in the Department of Psychiatry and the Department of Cell Biology at NYU Langone, as well as director of the Center for Dementia Research at Nathan Kline."

https://www.eurekalert.org/news-releases/954383

[Pipilongstocking]

Yep and why fasting is so good for the brain!

[nidan7500]

Excellent work Falconer. Maybe the Amyloid buildup thesis(root Cause of AD) will finally get the factual assessment it needs.

WELL DONE.He/She.! Not sure I could navigate that direct conflict with science on a regular bases.

This particular autophagy, removal of wastes inside cells, is compromised, which allows the accumulation of toxic wastes inside the cells, thereby disrupting normal cell functions. In brain cells, Alzheimer’s results.

“Our research suggests that future treatments should focus on reversing the lysosomal dysfunction and rebalancing acid levels inside the brain’s neurons,” says Nixon, a professor in the Department of Psychiatry and the Department of Cell Biology at NYU Langone, as well as director of the Center for Dementia Research at Nathan Kline.

[raja48185]

You might find this paper interesting. (About Mitophagy)

Comparing 2 agents that induce Mitophagy - UROLITHIN A (UA) vs NICOTINAMIDE MONONUCLEOTIDE (NMN)

https://www.nature.com/articles/s41419-022-04613-2

However, we found an interesting phenomenon that mitophagy activator UA, cannot alleviate mitochondrial fragmentation and dysfunction caused by PrP106-126, which eventually leads to cell apoptosis and decreased vitality. Based on reported studies [34], UA’s ability to prolong life and alleviate aging depends on mitochondrial function. We speculate that cells affected by prion disease have severe mitochondrial morphological fragmentation and dysfunction, so although UA can activate mitophagy, it also enhances damaged mitochondrial fragmentation. Then in that case, few functional mitochondria are left for UA to function in the neurons affected by the disease. Therefore, UA supplementation will not alleviate neuronal apoptosis and death caused by prion disease.

Another mitophagy activator, NMN supplementation could not only activate PINK1-parkin-mediated mitophagy in the prion disease cell model but also restore mitochondrial morphology and function, thereby alleviating neuronal apoptosis induced by PrP106-126, the therapeutic effect of NMN has also been reported in other diseases, such as premature aging-related ataxia telangiectasia and hypertension-related stroke [50, 51].

[jmvho]

Many thanks falconer!!

jmvho

[frrol]

This is not "New Evidence for Blarcamesine-induced Autophagy for Alzheimer’s." It's actually support for lysosomic (and potentially proteosomic) targets for AD and other neurodegeneration therapies, via protecting the proteosome. S-1 agonism has been shown in pre-clinical research (using 2-73, and other known agonists) to have upstream promotion of both implicated cellular mechanisms, so this latest research is encouraging for our drug.

Watch for trial results.