A pair of recent research results reinforce the idea that - with suitable engineering - the mental decline that occurs with aging can be can be greatly slowed or evaded. This is not repair, but it is a large improvement over the baseline. The work is in mice, which usually means the effects are more dramatic than when translated into human clinical therapies.
The researchers, appointed in the School of Medicine at The University of Texas Health Science Center San Antonio, added rapamycin to the diet of healthy mice throughout the rodents' life span. Rapamycin, a bacterial product first isolated from soil on Easter Island, enhanced learning and memory in young mice and improved these faculties in old mice, the study showed.
"We made the young ones learn, and remember what they learned, better than what is normal," said Veronica Galvan, Ph.D., assistant professor of physiology at the Barshop Institute for Longevity and Aging Studies, part of the UT Health Science Center. "Among the older mice, the ones fed with a diet including rapamycin actually showed an improvement, negating the normal decline that you see in these functions with age."
Given that rapamcyin was shown in that study to boost levels of neurotransmitters associated with neural plasticity, the first inclination would be to link the improved capabilities of the mice to increased growth and adaptability in neurons across the course of life. Further research will no doubt show whether that is a reasonable hypothesis.
Researchers from the University of Heidelberg had injected a virus that contains extra copies of the gene responsible for creating DNA methyltransferase into the hippocampus, area of the brain responsible for memory, of elderly mice that were showing signs of diminished memory. Afterwards, the team gave the mice a series of memory tests such as showing the mice a new object to investigate for a period of time, taking it away and presenting them with the same object the next day along with another new object.
Past studies showed that younger more able-minded mice will immediately begin investigating the newer object, while older mice will spend equal amounts of time investigating both objects, having seemingly forgotten that they'd already seen the object the day before.
The research team found that once the older mice were injected with the virus, the elderly mice had spent most of their time, 70 percent of the time, investigating the new object, suggesting that an increase of the enzyme restored their faulty memories to its original capacity. However, when researchers halved the amount of DNA methyltransferase produced by younger mice, the memory abilities deteriorated to that of non-treated older mice.
This second study gives a clear set of targets for the development of therapies that might benefit we humans - though bear in mind that in the present regulatory environment it takes a decade or two to move from a research result like this to clinical therapies, if the development process even manages to proceed that far. The costs imposed by the FDA and similar regulatory bodies make the establishment of a diverse development portfolio of possible therapies too expensive by far. Thus only the most likely and most broadly useful lines of research move deep into development - comparatively little of what may prove to be useful medicine is in fact taken far enough to be certain in this day and age.