{"id":557,"date":"2017-01-23T12:49:07","date_gmt":"2017-01-23T12:49:07","guid":{"rendered":"http:\/\/joshmitteldorf.peachpuff-wolverine-566518.hostingersite.com\/?p=557"},"modified":"2017-01-23T12:49:07","modified_gmt":"2017-01-23T12:49:07","slug":"first-fruits-of-research-with-young-blood-plasma","status":"publish","type":"post","link":"https:\/\/scienceblog.com\/joshmitteldorf\/2017\/01\/23\/first-fruits-of-research-with-young-blood-plasma\/","title":{"rendered":"First Fruits of Research with Young Blood Plasma"},"content":{"rendered":"

A recurrent theme on this page is the idea that human aging is driven by a combination of proteins circulating in the blood. \u00a0Blood is not just red cells and white cells; there is the blood plasma which contains thousands of dissolved proteins (and RNAs), signal molecules which regulate all aspects of metabolism, on time scales ranging from minutes to decades. \u00a0As we get older, the mix of these protein signals changes in ways that are relatively subtle, with less of some proteins and more of others. \u00a0It has been pretty well established<\/a> that the mix of proteins is characteristic of your age. \u00a0My bet is that the mix of proteins actually determines<\/i> your age, in the sense that changing the \u00a0blood plasma of an old person to that of a young person will, to a significant degree, transform the metabolism toward a younger state.<\/p>\n

The promise of this work came to prominence in parabiosis experiments with mice, beginning about 2005<\/a> out of Stanford. \u00a0Old mice were surgically paired with young mice, so their circulation was tied together. \u00a0The old mice become younger and the young mice became older. \u00a0In the intervening years, we have learned that blood plasma (no cells) from young animals has a rejuvenating effect on old animals.<\/p>\n

But giving old people frequent transfusions from young donors sounds like an experimental procedure for aging tycoons, not a practical plan for population-wide life extension. \u00a0Alternatively, to reproduce the full suite proteins in young blood artificially is a daunting task. \u00a0Are all<\/i> the proteins necessary for rejuvenation, or, perhaps, might the same success can be achieved with just a small number of proteins? \u00a0\u00a0Some would be added, others effectively subtracted from the blood by blocking their receptors with an inhibitor.<\/p>\n

So the race is on to find candidates for proteins in the blood that could be part of this small subset, a handful of proteins that might, if we\u2019re lucky, stand in for the thousands whose concentrations change with age. \u00a0The Stanford students from 2005 have graduated and now have labs of their own at Berkeley and Harvard \u00a0In the last few years, Mike and Irina Conboy of Berkeley<\/a> identified oxytocin as a key protein, and Amy Wagers at Harvard<\/a> identified GDF11, both proteins that we lose with age, and concentrations might be beefed up for rejuvenation. \u00a0Oxytocin is holding up; there is controversy about GDF11.<\/p>\n

But more effective than adding \u201cyouth factors\u201d to old blood may be removal<\/i> of pro-aging factors. \u00a0This was the preliminary finding<\/a> put out by the Conboys a few months ago. \u00a0Right around this time, from the lab of Tony Wyss-Coray at Stanford, came the first report of anti-aging benefits from blocking<\/i> a circulating protein. \u00a0VCAM-1<\/a> is a protein that increases with age, but has not previously been identified as a bad actor of primary import. \u00a0The \u201cCA\u201d in the middle of VCAM stands for cell adhesion<\/a>, an essential cell function which in itself is not good or bad. \u00a0Cells stick together for many reasons. \u00a0But VCAM-1 has been loosely linked in the past to cardiovascular disease and to arthritis.<\/p>\n

Hanadie Yousef, a post-doc at Wyss-Coray\u2019s Stanford lab, presented preliminary results at a Neuroscience meeting in November<\/a>, indicating that<\/p>\n