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Anti-Myostatin Antibody Treatment Increases Muscle Mass and Strength in Mice

As an alternative to myostatin gene therapy, treatments that temporarily block the action of myostatin have potential as a therapy to build muscle mass and strength. This is of particular interest as a way to compensate for sarcopenia, the characteristic loss of muscle that accompanies aging, and the approach is already in human trials. It is quite likely that such alternatives to gene therapy will reach the clinic first in more regulated regions, if only because they are favored by researchers and regulators for translation of genetic studies into the clinic. There is a tendency to researchers to look for approaches that require ongoing treatment to maintain, a tendency for pharmaceutical companies to want treatments that require ongoing expenditure rather than a one-time payment, and a tendency for regulators to endlessly delay anything related to gene therapy. Given the relentless advance of CRISPR, however, reducing costs and spreading the capability for gene therapy to many new labs and clinics, this will be happening at the very same time that gene therapies are available via medical tourism, I'll wager.

Sarcopenia, or aging-associated muscle atrophy, increases the risk of falls and fractures and is associated with metabolic disease. Because skeletal muscle is a major contributor to glucose handling after a meal, sarcopenia has significant effects on whole-body glucose metabolism. Despite the high prevalence and potentially devastating consequences of sarcopenia, no effective therapies are available.

Here, we show that treatment of young and old mice with an anti-myostatin antibody (ATA 842) for 4 weeks increased muscle mass and muscle strength in both groups. Furthermore, ATA 842 treatment also increased insulin-stimulated whole body glucose metabolism in old mice, which could be attributed to increased insulin-stimulated skeletal muscle glucose uptake as measured by a hyperinsulinemic-euglycemic clamp. Taken together, these studies provide support for pharmacological inhibition of myostatin as a potential therapeutic approach for age-related sarcopenia and metabolic disease.

Link: http://dx.doi.org/10.1073/pnas.1525795113

Comments

Hello! Does anybody know which is the last update from Liz Parrish? Is the myostation gene therapy working? Thanks!

Posted by: Josep at February 16th, 2016 8:30 AM

Thanks!!

Posted by: Josep at February 16th, 2016 1:02 PM

This is just a layperson's guess, but rather than antibodies to myostatin, it might be aptamers that take off. Singapore University recently demonstrated aptamers that apparently overcome past problems of being rapidly destroyed in the body by endonucleases and a lack of affinity at the binding site:

https://www.sciencedaily.com/releases/2016/02/160201085654.htm

As these can be cooked up in a test tube rather than in a complex cell based system, they'll probably wind up being much cheaper and easier to produce.

Posted by: Jim at February 17th, 2016 9:10 AM

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