Top Stories - Development & Aging

Dr. Thomas Brade
Vitamin A for the heart

Vitamin A is supposed to be really good for you – improving your vision, complexion and even...

Japanese fire belly newt (Cynops pyrrhogaster)
“Eye of newt”...

Contrary to long-held belief, at least one animal (the newt) can continue to regenerate tissue even...

heart muscle in a fruit fly (image courtesy of the Bodmer lab)
Marching to the same beat

A recent study from the Bodmer lab shows that fruit flies, mice, and humans all share a common...

Recycling fat to live longer?

by on September 6, 2011 at 9:00 am | 0 Comments
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Germline-less C. elegans nematodes with an autophagy marker shown in green. (Image courtesy of the Hansen lab)

Germline-less C. elegans nematodes with an autophagy marker shown in green. (Image courtesy of the Hansen lab)

Aging is generally accepted as a universal fact of life, but how do humans and other organisms age at the molecular level?

At Sanford-Burnham, a team led by Dr. Malene Hansen uses a type of worm called Caenorhabditis elegans to work out the molecular underpinnings of the aging process. Recently, they found that two cellular processes—lipid metabolism and autophagy—work together to influence worms’ lifespan. Autophagy, a major mechanism cells use to digest and recycle their own contents, has become the subject of intense scientific scrutiny over the past few years, particularly since the process (or its malfunction) has been implicated in many human diseases, including cancer and Alzheimer’s disease. (See Autophagy 101.)

The Hansen group’s latest study, published online September 8 in Current Biology, provides a more detailed understanding of the roles autophagy and lipid metabolism play in aging.

“The particular worm model we used in this study is known to live longer than normal worms, but we didn’t completely understand why,” said Dr. Hansen, assistant professor in Sanford-Burnham’s Del E. Webb Neuroscience, Aging and Stem Cell Research Center and senior author of the study. “Our results suggest that increased autophagy has an anti-aging effect, possibly by promoting the activity of a fat-digesting enzyme. In other words, it seems that recycling fat is a good thing—at least for worms.”

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Marching to the same beat

by on August 4, 2011 at 11:23 am | 0 Comments
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heart muscle in a fruit fly (image courtesy of the Bodmer lab)

heart muscle in a fruit fly (image courtesy of the Bodmer lab)

Heart disease is the leading cause of death in the United States, accounting for more than 25 percent of all deaths each year. While many factors work together to contribute to heart disease—including environment, lifestyle, and genetics—we only have control over the first two. To address the third factor (genetics), researchers at Sanford-Burnham recently turned to fruit flies.

Fly and human genes are so closely related that the sequences of newly discovered human genes, including many that contribute to disease, can often be matched up with fly counterparts. Since fruit flies are relatively easy to work with (they’re small, breed quickly, and don’t require a lot of maintenance), they often give scientists clues to the functions of human genes and helps them develop drugs that target them.

As Dr. Rolf Bodmer, director of Sanford-Burnham’s Development and Aging Program, explains in the Journal of Cell Biology, “We use fruit flies to learn about the fundamental genetic mechanisms that are important for the development and function of the heart.”

Dr. Bodmer himself discovered early in his career that flies lacking Tinman, a protein that regulates the expression of other genes, fail to develop heart tissue during embryonic development. If Tinman is removed later during fly development, the flies’ hearts don’t function properly.

Now researchers in Dr. Bodmer’s lab, led by postdoctoral researcher Dr. Li Qian, uncovered a genetic network that controls heart development and function in fruit flies and mice, with additional clues that it might also play a role in human heart health.

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“Eye of newt” reverses a long-held scientific dogma

by on July 12, 2011 at 8:57 am | 0 Comments
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Japanese fire belly newt (Cynops pyrrhogaster)

Japanese fire belly newt (Cynops pyrrhogaster)

For nearly 250 years, generations of scientists believed that the older an animal gets, the less able it is to regenerate and replace damaged or diseased tissue. (Even Charles Darwin weighed in.) Everyone assumed that, as animals age, cellular resources become exhausted, DNA repair mechanisms break down, healing takes longer and tumors develop. As of today, however, that’s no longer the doctrine. It still might be harder and harder for humans to repair wounds and heal as we age, but it turns out that the humble newt is another story.

When injured, newts can regenerate limbs, tails or eyes right back to factory standards. Humans can only do that at the very tip of the finger and only under very limited circumstances. And according to a new study published today in the journal Nature Communications, old newts can do it just as well as young newts. The study focused on the newt’s optical lens, which can be removed entirely and, after the incision heals, completely regenerate in a single day. The study’s lead author, Dr. Goro Eguchi, began breeding newts and collecting lenses 16 years ago. Throughout the years since, lenses were removed 18 times from the same animals. By the time of the last tissue collection, they were at least 30 years old (very old, for a newt).

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Vitamin A for the heart

by on January 26, 2011 at 4:16 pm | 2 Comments
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Dr. Thomas Brade

Dr. Thomas Brade, post-doctoral researcher in the Duester lab, studies retinoic acid and development.

Vitamin A is supposed to be really good for you – improving your vision, complexion and even pre-natal health. But what does it do, exactly?

“That’s actually not very well known,” says Dr. Gregg Duester, professor in Sanford-Burnham’s Development and Aging program. “For example, even though it’s been clear for 100 years that vitamin A is required for proper embryonic development, only now are we getting to the molecular details of what it does.”

Researchers in Dr. Duester’s lab study retinoic acid, an active form of vitamin A. They are especially interested in understanding how retinoic acid tells the right body parts to form in the right places at the right time in a developing embryo. Recently, while comparing limb buds (the precursors of arms and legs) in mice with – and without – the ability to generate retinoic acid from vitamin A, they decided to check out the differences in their hearts, too. As it turns out, the ventricles (the part of the heart that pumps blood out to the rest of the body) in retinoic acid-deficient mouse embryos, were thinner than those in their normal counterparts.

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