Thomas Rando and Anne Brunet provide a general overview on the process and potential prevention of aging. The topics they cover vary from symptoms of aging to unusual characteristics that seem to prolong longevity.
Stanford Mini Med School is a series arranged and directed by Stanford’s School of Medicine and presented by the Stanford Continuing Studies program.
By Louis Bergeron
STANFORD, Calif. — Communication is critical. Garbled in, garbled out, so to (mis-)speak. Workers who get incomplete instructions produce an incomplete product, and that’s exactly what happens with the stem cells in our aging muscles, according to researchers from the Stanford University School of Medicine.
Their study found that, as we age, the lines of communication to the stem cells of our muscles deteriorate and, without the full instructions, it takes longer for injured muscles to heal. Even then, the repairs aren’t as good. But now that the researchers have uncovered the conduit that conveys the work orders to muscle stem cells, that knowledge could open the door to new therapies for injuries in a host of different tissues.
The findings, from the lab of Thomas Rando, MD, PhD, associate professor of neurology and neurological sciences, suggest stem cells are careful when they undergo cell division so that random mutations in their chromosomes are not passed on to the next generation of stem cells. The results support a much-debated hypothesis proposed in 1975 by Oxford University geneticist John Cairns, PhD. Although other groups have uncovered hints that Cairns was right, Rando’s findings are the most detailed to date.
The results are published in the April 17 issue of the Public Library of Science-Biology.
Rando said no other work he’s done has created as much excitement among his colleagues in the stem cell field. “The lesson from this is that when something seems strange, don’t ignore it. Sometimes what puzzles you turns out to be the most interesting,” he said.
STANFORD, Calif. — A new gene therapy technique that has shown promise in skin disease and hemophilia might one day be useful for treating muscular dystrophy, according to a new study by researchers at Stanford University School of Medicine.
In the study, published online in the Proceedings of the National Academy of Sciences the week of Jan. 2, the researchers used gene therapy to introduce a healthy copy of the gene dystrophin into mice with a condition that mimics muscular dystrophy. The dystrophin gene is mutated and as a result produces a defective protein in the roughly 20,000 people in the United States with the most common form of the disease.
BY LOUIS BERGERON
Three School of Medicine scientists, including one jointly appointed with the School of Engineering, are among a select group of 13 researchers nationwide being recognized for their innovative work by the National Institutes of Health. The winners of the NIH Director’s 2005 Pioneer Awards will each receive up to $500,000 annually for five years to help fund their research.
With three winners, Stanford has more awardees this year than any other institution. The NIH announced the winners on Sept. 29. “Although the Pioneer Award is relatively new, it has quickly become one of the most prestigious and important recognitions by the NIH,” said Philip Pizzo, MD, dean of the School of Medicine. “Having three Pioneer Award winners is simply remarkable.”
STANFORD – Any older person can attest that aging muscles don’t heal like young ones. But it turns out that’s not the muscle’s fault. A study in the Feb. 17 issue of Nature shows that it’s old blood that keeps the muscles down.
The study, led by Thomas Rando, MD, PhD, associate professor of neurology and neurological sciences at the Stanford University School of Medicine, built on previous work showing that old muscles have the capacity to repair themselves but fail to do so. Rando and his group studied specialized cells called satellite cells, the muscle stem cells, that dot muscle tissue. These normally lie dormant but come to the rescue in response to damaged muscle-at least they do in young mice and humans.