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Researchers from the Harvard Stem Cell Institute (HSCI) have shown that injections of a protein dubbed GDF11, when administered to older mice, appear to cause a reversal of many signs of aging. Analysis showed that every major organ system tested displayed signs of improvement, with the protein even appearing to reverse some of the DNA damage which is synonymous with the aging process itself.

The protein GDF11 is found in humans as well as mice, and is now being considered for possible human testing due to its surprising and apparently regenerative properties.

A previous study had focused on examining the hearts of mice the equivalent of 70 human years old. The mice were regularly exposed to the blood of younger mice whose blood carried a higher concentration of GDF11. Ordinarily the hearts of older mice are enlarged and weakened, however results from the previous study displayed that, thanks to the GDF11 protein present in the blood of the younger mice, the hearts of the elderly mice reduced in size, making them appear younger and healthier. The changes were not purely aesthetic however, with the mice displaying an increased ability to exercise for prolonged periods of time.

The most recent set of experiments tested the protein in two ways. The first stage of the testing involved linking the circulatory systems of an older and a younger mouse through what is known as a parabiotic system. This allowed the protein-rich blood from the younger mouse to flow through the elder's system continuously, maximizing the effect of the protein. The second method involved injecting the older mice with a concentrated dose of GDF11.

Results from the second study showed that the protein had positive effects reaching far beyond the heart. It was found that, having been exposed to increased levels of the protein, all organs examined by the researchers displayed a heightened level of function. Furthermore, whilst previous studies on the protein had focused on regenerating damaged muscle in mice, the most recent study focused on the repair of cells damaged by the aging process. The GDF11 protein was found to reverse some of this damage, allowing muscle to function as effectively as that of a much younger mouse.

Analysis of the brains of the older mice via MRI imaging displayed an increase in neural stem cells along with the development of blood cells in the brain. “There seems to be little question that, at least in animals, GDF11 has an amazing capacity to restore aging muscle and brain function,” states Dr. Doug Melton, co-chair of HSCI. The team believes that due to the increased blood flow exhibited in the brain of the elderly mice, it may be possible to reverse some of the cognitive effects of aging. The protein was also found to improve the olfactory system of older mice, greatly heightening their sense of smell.

In terms of human applications, it is hoped that a drug derived from GDF11 will lead to a cure for conditions such as diastolic heart failure. This condition is a defect which eventually causes one or more of the ventricles of the heart to deteriorate while attempting to fill the heart with blood, in order to pump it around the body. There is also a possibility that a GDF11-inspired drug could be used to combat Alzheimer's, a condition synonymous with the aging process.

Looking to the future, the team will continue studies of the GDF11 protein, with a view to begin human medical trials within three to five years.

The research papers regarding the discoveries surrounding GDF11 are available in the journal Science.

Related Link:

J. Kaiser, “‘Rejuvenation Factor’ in Blood Turns Back the Clock in Old Mice,” Science344, 6184 (9 May 2014).                        

L. Katsimpardi et al., “Vascular and Neurogenic Rejuvenation of the Aging Mouse Brain by Young Systemic Factors,” Science344, 6184 (9 May 2014).                        

M. Sinha et al., “Restoring Systemic GDF11 Levels Reverses Age-Related Dysfunction in Mouse Skeletal Muscle,” Science344, 6184 (9 May 2014).                        

S. S. Hall, “Young blood,” Science345, 6202 (12 September 2014).