Anavex Life Sciences Corp (AVXL)

[nidan7500]

Good to see this kind of work paying off, even if it is exactly what BIIB...FDA etal do not want to hear. How does a large group of highly trained/skilled and very smart people end up on the wrong track-(DEAD ENDED) after decades of research??)


https://flip.it/NwI46q Decreased Proteins, Not Amyloid Plaques, Tied To Alzheimer’s Disease

Next steps
Sturchio said the research is moving forward to study if increasing the levels of soluble amyloid-beta in the brain is a beneficial therapy for patients with Alzheimer’s.

Espay said it will be important to ensure that the elevated levels of the protein introduced into the brain do not then turn into amyloid plaques, since the soluble version of the protein is needed for normal function to make an impact in the brain.

On a larger scale, the researchers said they believe a similar hypothesis of what causes neurodegeneration can be applied to other diseases including Parkinson’s and Creutzfeldt-Jakob disease, with research ongoing in these areas as well.

For example, in Parkinson’s disease, a normal soluble protein in the brain called alpha-synuclein can harden into a deposit called a Lewy body. The researchers hypothesize that Parkinson’s is not caused by Lewy bodies aggregating in the brain, but rather by a decrease in levels of normal, soluble alpha-synuclein.

“We’re advocating that what may be more meaningful across all degenerative diseases is the loss of normal proteins rather than the measurable fraction of abnormal proteins,” Espay said. “The net effect is a loss not a gain of proteins as the brain continues to shrink as these diseases progress.”

Espay said he envisions a future with two approaches to treating neurodegenerative diseases: rescue medicine and precision medicine.

Rescue medicine looks like the current work, studying if boosting levels of key proteins like amyloid-beta leads to better outcomes.

“Interestingly, lecanemab, the anti-amyloid drug recently reported as beneficial, does something that most other anti-amyloid treatments don’t do in addition to reducing amyloid: it increases the levels of the soluble amyloid-beta,” Espay said.

Alternatively, precision medicine entails going deeper to understand what is causing levels of soluble amyloid-beta to decrease in the first place, whether it is a virus, a toxin, a nanoparticle or a biological or genetic process. If the root cause is addressed, the levels of the protein wouldn’t need to be boosted because there would be no transformation from soluble, normal proteins to amyloid plaques.

Espay said precision medicine would take into account the fact that no two patients are alike, providing more personalized treatments. The researchers are making progress in precision medicine through the Cincinnati Cohort Biomarker Program, a project aiming to divide neurodegenerative diseases by biological subtypes in order to match therapies based on biomarkers to those most likely to benefit from them.

FINALLY....With any luck, we may now add the ole (Dr. Peter Senge list of things we know , we know). "AMYLOID PLAQUE", thesis onto the list of things we now "KNOW WE KNOW"....IT IS NOT THE CAUSE OF AD...IT'S DEAD AND WE KNOW IT"S DEAD..... NICE.

Also worth noting, AVXL MOA IS ALIVE AND WELL....Sure am happy that we have a patent on our new MOA ...now, let's get to work and apply it in CNS science apps , WW. Including those pesky RARE Diseases....finally, we can help people put their BIO_SCIENCE knowledge to productive use .