Replies to post #215338 on Anavex Life Sciences Corp (AVXL)

[XenaLives]

The article concludes:

He further explained that metabolic and mitochondrial dysfunctions should be viewed as fundamental features of aging in general and that age-dependent diseases, including Alzheimer’s, should, therefore, be viewed as manifestations of aging. Hence, it may be easier to prevent or treat age-dependent diseases by targeting the mechanisms of aging rather than treating individual diseases after symptoms occur.

https://www.genengnews.com/news/metabolic-mitochondria-dysfunction-may-be-primary-cause-of-alzheimers/

[nidan7500]

polarbear

Very interesting and important (for Anavex) publication released yesterday 10/18/19. Thank you georgegii.

“Metabolic Mitochondria Dysfunction May Be Primary Cause of Alzheimer’s
A team of researchers led by Yale-NUS College says it has found evidence that metabolic dysfunction is a primary cause of Alzheimer’s disease.”
https://www.genengnews.com/news/metabolic-mitochondria-dysfunction-may-be-primary-cause-of-alzheimers/


And just 5 days ago Alzheimer’s News Today has this to say about our compound:

“Anavex 2-73 is a small molecule that activates the sigma-1 receptor, which is known to modulate cellular processes relevant to neurodegeneration. Specifically, Anavex 2-73 is thought to help restore cellular balance by targeting protein misfolding (when proteins fail to fold correctly, into a normal configuration, they do not work as intended), oxidative stress (which damages cells due oxygen molecules with free radicals, or unpaired electrons), mitochondrial dysfunction, inflammation, and cellular stress.”

https://alzheimersnewstoday.com/anavex-2-73/

The picture is coming more and more into focus. At least for those willing to think clearly.

Bear,
It would be nice to see this compiled fact set as evidence the "SYSTEM" is beginning to "Turn into the wind" (getting ready for action). It may be that various related-supportive pubs from through out the medical/academic community are seeing the light and are positioned to support the Peer reviewed PUB we have heard so much about. Maybe I am just seeing the wrong vision but .."it could happen". IMO, they all have to cover their asses before the bomb gets dropped.

I am not a conspiracy theory guy but I do ask WHY al lot. The academic and big thinkers have massive egos and have to appear to have been in the room (virtually) when the light gets turned on.. IMO, none of these actions are anecdotal, all linked/connected as planned.

[pcguy]

Graphical summary of the model of Aß pathology in GRU102.

Graphical Summary

Pan-neuronal Aß expression leads to an imbalance between reactive oxygen species (ROS) production and antioxidant (AOX) defense, resulting in oxidative stress as an early event in GRU102. Increase in mitochondrial protein carbonyl content (mtPCC) was also observed as an early phenomenon in GRU102. Elevated oxidative stress further affects ROS-sensitive Tricarboxylic Acid (TCA) cycle enzyme, including alpha-ketoglutarate dehydrogenase (aKGDH), resulting in a reduction of its activity as well as altered levels of TCA metabolites (aKGDH, fumarate and malate) in old GRU102. Together with the reduction in electron transfer chain (ETC) complex I and IV activities as well as low ATP levels in the GRU102 animals we reported previously (Fong et al., 2016), these phenomena result in metabolic stress. Proteostasis, an energy-intensive process, is impaired by metabolic and oxidative stress, resulting in an increase in general protein aggregates. Treatment with Metformin (Met) increases stress resistance and rescues metabolic defects of GRU102. Metformin-treated GRU102 also appears to reduce the increase in protein aggregates in GRU102, even though it could not fully rescue this phenotype.

https://doi.org/10.7554/eLife.50069.025

Didn't someone ask about oxidative stress?

[makemydaze]

Add the NINDS researchers to that picture - also from 5 days ago:

"The National Institute of Neurological Disorders and Stroke (NINDS) has awarded a five-year, $20 million grant to researchers looking for a way to image misfolded proteins in the brains of people with Parkinson’s and other neurodegenerative diseases, which could greatly advance diagnosis and disease monitoring.

Parkinson’s disease is thought to be a proteinopathy — a condition caused by proteins in the brain folding improperly, which sets off a chain reaction of misfolding in other proteins, eventually forming clumps and damaging the brain. Specifically, Parkinson’s is characterized by clumps of the protein alpha-synuclein.

Alzheimer’s disease is another proteinopathy, characterized by clumps of beta-amyloid. But there’s a crucial difference between the two in terms of how they are diagnosed and managed.

Brains can be imaged using a positron emission tomography (PET) scan, a technique in which a radioactive dye called a tracer is injected into the body. The tracer then binds to specific proteins, allowing clumps of these proteins to be visible on the scan. Although PET scans have been able to image beta-amyloid plaques for nearly a decade, the technology to visualize clumps of alpha-synuclein doesn’t yet exist."

https://parkinsonsnewstoday.com/2019/10/14/20-million-grant-awarded-study-imaging-protein-misfolding-parkinsons/

Is Anavex going to be able to use the positive bacterial changes in the gut as a biomarker?