Anavex Life Sciences Corp (AVXL)

[sokol]

Biomarkers are an important factor the FDA may consider in approving a drug. Can someone explain the biologic measures (biomarkers) Dr. Norman Relkin referred to regarding the recent AVXL data. I have done some research that I refer to below separated by ***

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Dr. Norman Relkin said this about the July AVXL 2-73 data: "It also provided encouraging evidence that previously reported positive trends in certain cognitive and biologic measures persisted over a period of approximately 31 weeks. "

https://globenewswire.com/news-release/2016/07/29/860192/0/en/Anavex-Confirms-Data-from-Phase-2a-Study-of-ANAVEX-2-73-in-Alzheimer-s-Patients-Presented-at-AAIC-2016.html

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Dr. Relkin is 'a co-inventor on the patent entitled "Multiplexed Cerebrospinal Fluid Markers for Alzheimer's disease" that is assigned to the Cornell Research Foundation.'

https://www.alzforum.org/member-directory/norman-relkin

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See this article: The evolution of amyloid toxicity in Alzheimer's -- ScienceDaily
'Outsized human suffering is linked to 'amyloid beta,' an otherwise tiny, innocuous-looking protein molecule, as it is suspected to be a key player in neurodegenerative mechanisms underlying Alzheimer's disease. The molecules appear to become toxic within our bodies when they make contact with each other and form small bundles. Oddly, they may become less toxic again as the bundles grow and form ordered fibrillary plaque deposits. This begs the question: what's different about these bundles?"'
https://www.sciencedaily.com/releases/2016/03/160301144750.htm

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Antibodies could be key defenders against Alzheimer's, new evidence shows:
By Jonathan Weil
In a major advance in the battle against Alzheimer's disease and related forms of dementia, researchers at NewYork-Presbyterian Hospital/Weill Cornell Medical Center have identified naturally occurring antibodies in human blood that may help defend against the buildup of harmful plaques in the brain.

The newly found antibodies selectively target aggregates of beta amyloid proteins that are toxic to brain cells, while ignoring the benign single-molecule forms of the same proteins. The existence of such antibodies was predicted by animal studies, but they were never previously demonstrated to be present in substantial quantities in blood from normal humans.

Lead researcher Norman Relkin, a behavioral neurologist and neuroscientist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center, presented the findings at the second Alzheimer's Association International Conference on Prevention of Dementia, June 11 in Washington, D.C.
http://www.news.cornell.edu/stories/2007/06/antibodies-could-defend-against-alzheimers-researchers-show

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In the transgenic amyloid expressing mouse model Tg2576, where the sigma-1 receptor (S1R) expression is impaired through S1R KO (knock out), at 12 months the survival was reduced by 50% compared to the non-S1R KO Tg2576 model. Apparently the genetic inactivation of the S1R gene worsens amyloid toxicity and has a detrimental impact on survival and also memory impairment. Amyloid is believed to play a key role in the development of the symptoms of Alzheimer’s disease (AD). On the other hand, activation of the S1R through treatment with the S1R agonist ANAVEX 2-73 in the Tg2576 model alleviates amyloid toxicity and resulting learning deficits both after one month and two months daily oral treatment, respectively. In addition expression of ROS (reactive oxidative species) as well as plasticity related IEG and transcription factors in the mouse hippocampus were clearly negatively impacted through the S1R KO, however, were significantly improved through ANAVEX 2-73. This confirms that targeting the S1R, a key factor in brain plasticity, may demonstrate neuroprotection in Alzheimer’s disease. ANAVEX 2-73 is currently undergoing a Phase 2a trial in Alzheimer’s patients.
http://www.anavex.com/?news=anavex-presents-positive-results-for-both-anavex-2-73-and-anavex-3-71-in-alzheimers-models-at-2015-adpd-conference

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ANAVEX 2-73 demonstrated to be effective on functional responses and biochemical markers of the toxicity developed in Tg2576 mice. Interestingly, the compound only marginally decreased soluble amyloid-beta brain contents. Since many therapeutic strategies based on lowering amyloid-beta have failed, it is quite possible that amyloid-beta reduction does not correlate directly with disease improvement.

http://www.anavex.com/?news=anavex-announces-positive-data-for-anavex-2-73-in-alzheimers-disease