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Exercise Releases Brain-Healthy Protein

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ExerciseWe all know that exercise is important for a strong and healthy body. Less appreciated is that exercise seems also to be important for a strong and healthy mind, boosting memory and learning, while possibly delaying age-related cognitive decline [1]. How is this so? Researchers have assembled a growing body of evidence that suggests skeletal muscle cells secrete proteins and other factors into the blood during exercise that have a regenerative effect on the brain.

Now, an NIH-supported study has identified a new biochemical candidate to help explore the muscle-brain connection: a protein secreted by skeletal muscle cells called cathepsin B. The study found that levels of this protein rise in the blood of people who exercise regularly, in this case running on a treadmill. In mice, brain cells treated with the protein also exhibited molecular changes associated with the production of new neurons. Interestingly, the researchers found that the memory boost normally provided by exercise is diminished in mice unable to produce cathepsin B.


Creative Minds: A New Chemistry for Aging Research?

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Tony Wyss-Coray

Tony Wyss-Coray / Credit: Stanford School of Medicine

Basic scientists have long studied aging by looking inside of cells. While this research has produced many important leads, they are now starting to look outside the cell for the wealth of biochemical clues contained in the bloodstream.

To introduce you to this exciting frontier in aging research, this blog highlighted a while back the work of Tony Wyss-Coray at Stanford School of Medicine, Palo Alto, CA. He and a colleague had just received a 2013 NIH Director’s Transformative Research Award to explore the effects of exercise on the brains of mice. Their work, in fact, produced one of Science Magazine’s Breakthrough Discoveries of 2014. Their team showed that by fusing the circulatory systems of old and young mice to create a shared blood supply, the young blood triggered new muscle and neural connections in the older mice, while also improving their memories.

As fascinating as this theoretical Fountain of Youth was, Wyss-Coray recognized a critical limitation. He had no way of knowing how factors secreted by the young mouse could actually cross the blood-brain barrier and rejuvenate neurons. To solve this unknown, Wyss-Coray recently received a 2015 NIH Director’s Pioneer Award to build a potentially game-changing tool to track the aging process in mice.


Less TOR Protein Extends Mouse Lifespan

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Mouse walking towards a fountainThe average life expectancy in the United States currently is about 79 [1]. And, unsurprisingly, more than two-thirds of Americans say they’d like to live another 10 to 20 years longer [2].

One possible route to a longer life is to cut calories drastically. Not much fun perhaps, but there’s evidence it works in yeast, worms, and mice—but probably not in monkeys [3]. The potential life-extending strategy that I’d like to tell you about today focuses on the drug rapamycin, which blocks the activity of a protein called “target of rapamycin,” or TOR. Recently, a team here at NIH discovered that—at least in mice—reducing production of this protein through genetic engineering can add about 20% to the lifespan [4].


Reprogramming Genes to Keep Joints Healthy

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Caption: [Left] The knee joint of a normal mouse that endured an ACL-type injury. The injury triggered osteoarthritis and caused the cartilage on the femur (red) and tibia (green) to degrade, allowing the bones to sandwich together. [Right] This is the knee joint of a mouse that received gene therapy after the ACL injury. The cartilage is thick and healthy, and covers the bones completely, providing a cushion.

Credit: Brendan Lee and Zhechao Ruan, Department of Molecular and Human Genetics,
Baylor College of Medicine, Houston, TX

Our joints are pretty amazing marvels of engineering, but they don’t last forever. As we age, or if we suffer certain injuries, the smooth, slippery white cartilage covering the ends of our bones begins to fray and degrade. This causes osteoarthritis (OA), or ‘wear-and-tear’ arthritis. As the cartilage thins and disappears, the bones can even grow spurs that grate against each other, causing swelling and pain. It’s a major cause of disability, and there’s currently no cure—other than joint replacement, which is a pretty big deal and isn’t available for all joints. About 27 million Americans already have osteoarthritis; about 1 in 2 will suffer from some form of the disease over their lifetime. Those are lousy odds.


Of Mice, Men, and Medicine

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Photo of someone holding the lab on a chip device next to a photo of two laboratory mice

Will a chip challenge the mouse?
Source: Wyss Institute and Bill Branson, NIH

The humble laboratory mouse has taught us a phenomenal amount about embryonic development, disease, and evolution. And, for decades, the pharmaceutical industry has relied on these critters to test the safety and efficacy of new drug candidates. If it works in mice, so we thought, it should work in humans. But when it comes to molecules designed to target a sepsis-like condition, 150 drugs that successfully treated this condition in mice later failed in human clinical trials—a heartbreaking loss of decades of research and billions of dollars. A new NIH-funded study [1] reveals why.


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