Sunday, December 06, 2015 6:34:03 PM
Scientists used to believe that aging was caused by mutations in the genetic blueprint of the cells – a theory that, according to Dr. David Sinclair (see below) , may still apply in later life – but if the earlier phases of aging are caused by a drop-off in NAD+ levels, as Dr. Sinclair’s research indicates, some aspects of aging could theoretically be reversed.
David Sinclair, Ph.D. is Co-Director of the Paul F. Glenn Center for the Biology of Aging, a Professor of Genetics at Harvard Medical School, Associate Member of the Broad Institute for Systems Biology, and co-founder of Sirtris Pharmaceuticals, Waltham, MA. Dr. Sinclair’s research aims to identify conserved longevity control pathways and devise small molecules that activate them, with a view to preventing and treating diseases caused by aging. His lab was the first to identify small molecules called STACs that can activate the SIRT pathway and extend lifespan of a diverse species. They also discovered key components of the aging regulatory pathway in yeast and is now focused on finding genes and STACs that extend the healthy lifespan.
According to Wikipedia:
"Sirtris Pharmaceuticals, Inc. was a biotechnology company based in Cambridge, MA that developed therapies for type 2 diabetes, cancer, and other diseases. Founded in 2004 by Harvard University biologist David Sinclair, venture capitalist Christoph Westphal, and serial entrepreneur Andrew Perlman, the company went public in 2007 and was subsequently purchased by GlaxoSmithKline in 2008 for $720 million. It was operated as a business unit of GSK until 2013, when it was absorbed into GSK, where research and development continues.[1] Sirtris's drug discovery was focused on developing activators of sirtuins, a class of enzyme that may mediate benefits of calorie restriction. The company's current lead candidates are SRT2104 and SRT2379, which are both potent activators of the SIRT1 enzyme. These and related molecules are in clinical development. The company's other drug candidate was SRT-501, a proprietary formulation of the compound resveratrol, possibly an activator of the SIRT1 enzyme.[2] Development of SRT-501 was halted by GlaxoSmithKline in late 2010, due to suspected drug-related adverse effects in study participants. The company later focused on developing more potent synthetic activators of SIRT1 and is investigating SIRT3 as another potential drug target.[3] Studies from rivals Amgen and Pfizer cast doubt on whether SIRT1 was directly activated.[4][5] Subsequent work provided evidence that the original conclusions of Sinclair were correct: SIRT1 is directly activated by resveratrol and the synthetic activators, with the activator binding in the N-terminus of SIRT1.[6] A mutation in this N-terminal SIRT1 domain (SIRT1-E230K) was shown to block activation by resveratrol and by synthetic activators from Sirtris, both in vitro and in vivo, largely settling the scientific debate. In 2014, SRT1720 and SRT2104 were shown to extend the health span and the lifespan of mice on a standard diet."
See Seeking Alpha article "Anavex 2-73: How It May Work" $AVXL. http://www.seekingalpha.com/article/3734766
This article concludes that IF Anavex 2-73 is a, "particularly good hydrogen donor" it may reverse damage that oxidation and nitration has done thereby reversing AZ?
See also:
http://www.npr.org/sections/health-shots/2015/03/09/390980364/mad-cow-research-hints-at-ways-to-halt-alzheimers-parkinsons
"What we found is that if you replenish NAD in these neurons, it completely protects them against the injury caused by misfolded prion protein," Lasmezas says.
That suggests the right drugs could protect brain cells from the misfolded proteins involved in Alzheimer's and Parkinson's and ALS, Lasmezas says."
See https://en.m.wikipedia.org/wiki/Hydrogen_carrier. NAD is a hydrogen carrier.
Could it be that Anavex 2-73 may be a hydrogen carrier or it may replenish NAD (a hydrogen carrier) in neurons? Can someone more knowledgeable explain this?
Below is a couple of paragraphs from the internet about hydrogen carriers and the role they play in the body.
A hydrogen carrier is an organic macromolecule that transports atoms of hydrogen from one place to another inside a cell or from cell to cell for use in various metabolical processes. An example is NADPH in photosynthesis also called NAD along with it FAD is also one of the hydrogen carriers.The main role of these is to transport hydrogen atom to electron transport chain which will change ADP to ATP by adding one phosphate.
Adenosine triphosphate (ATP) is considered by biologists to be the energy currency of life. It is the high-energy molecule that stores the energy we need to do just about everything we do. It is present in the cytoplasm and nucleoplasm of every cell, and essentially all the physiological mechanisms that require energy for operation obtain it directly from the stored ATP. (Guyton) As food in the cells is gradually oxidized, the released energy is used to re-form the ATP so that the cell always maintains a supply of this essential molecule. Karp quotes an estimate that more than 2 x 1026 molecules or >160kg of ATP is formed in the human body daily! ATP is remarkable for its ability to enter into many coupled reactions, both those to food to extract energy and with the reactions in other physiological processes to provide energy to them. In animal systems, the ATP is synthesized in the tiny energy factories called mitochondria by a process called glycolysis.
Maybe someone here can make more sense of all this, but it does seem that, according to Corinne Lasmezas, replinishing NAD
In neurons protects them against injury. NAD tends to diminish as we age. AZ is a disease prevalent in the elderly. The Seeking Alpha article published last week "Anavex and How it May Work" seems to be related to what Lasmezas said in the Mad Cow article re NAD.
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