Brain Cells Found To Control Aging

Scientists at Albert Einstein College of Medicine have found that stem cells in the brain’s hypothalamus govern how fast aging occurs in the body. The finding, made in mice, could lead to new strategies for warding off age-related diseases and extending lifespan. The hypothalamus was known to regulate important processes including growth, development, reproduction and metabolism. In a 2013 Nature paper, Einstein researchers made the surprising finding that the hypothalamus also regulates aging throughout the body. Now, the scientists have pinpointed the cells in the hypothalamus that control aging: a tiny population of adult neural stem cells, which were known to be responsible for forming new brain neurons.

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Our research shows that the number of hypothalamic neural stem cells naturally declines over the life of the animal, and this decline accelerates aging,” says senior author Dongsheng Cai, M.D., Ph.D., professor of molecular pharmacology at Einstein. “But we also found that the effects of this loss are not irreversible. By replenishing these stem cells or the molecules they produce, it’s possible to slow and even reverse various aspects of aging throughout the body.”

The findings have been published online in Nature.

Source: http://www.einstein.yu.edu/
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http://www.reuters.com/

One Molecule Plays David Against The Goliath Of Aging

Are pomegranates really the superfood we’ve been led to believe will counteract the aging process? Up to now, scientific proof has been fairly weak. And some controversial marketing tactics have led to skepticism as well. A team of scientists from Ecole Polytechnique Fédérale de Lausanne (EPFL) in Switzerland and the company Amazentis wanted to explore the issue by taking a closer look at the secrets of this plump pink fruit. They discovered that a molecule in pomegranates, transformed by microbes in the gut, enables muscle cells to protect themselves against one of the major causes of aging. In nematodes and rodents, the effect is nothing short of amazing. Human clinical trials are currently underway, but these initial findings have already been published in the journal Nature Medicine. 

pomegranates

As we age, our cells increasingly struggle to recycle their powerhouses. Called mitochondria, these inner compartments are no longer able to carry out their vital function, thus accumulate in the cell. This degradation affects the health of many tissues, including muscles, which gradually weaken over the years. A buildup of dysfunctional mitochondria is also suspected of playing a role in other diseases of aging, such as Parkinson’s disease.
The scientists identified a molecule that, all by itself, managed to re-establish the cell’s ability to recycle the components of the defective mitochondria: urolithin A. “It’s the only known molecule that can relaunch the mitochondrial clean-up process, otherwise known as mitophagy,” says Patrick Aebischer, co-author on the study. “It’s a completely natural substance, and its effect is powerful and measurable.”

The team started out by testing their hypothesis on the usual suspect: the nematode C. elegans. It’s a favorite test subject among aging experts, because after just 8-10 days it’s already considered elderly. The lifespan of worms exposed to urolithin A increased by more than 45% compared with the control group.

These initial encouraging results led the team to test the molecule on animals that have more in common with humans. In the rodent studies, like with C. elegans, a significant reduction in the number of mitochondria was observed, indicating that a robust cellular recycling process was taking place. Older mice, around two years of age, showed 42% better endurance while running than equally old mice in the control group.

According to study co-author Johan Auwerx, it would be surprising if urolithin A weren’t effective in humans. “Species that are evolutionarily quite distant, such as C elegans and the rat, react to the same substance in the same way. That’s a good indication that we’re touching here on an essential mechanism in living organisms.”

Urolithin A’s function is the product of tens of millions of years of parallel evolution between plants, bacteria and animals. According to Chris Rinsch, co-author and CEO of Amazentis, this evolutionary process explains the molecule’s effectiveness: “Precursors to urolithin A are found not only in pomegranates, but also in smaller amounts in many nuts and berries. Yet for it to be produced in our intestines, the bacteria must be able to break down what we’re eating. When, via digestion, a substance is produced that is of benefit to us, natural selection favors both the bacteria involved and their host. Our objective is to follow strict clinical validations, so that everyone can benefit from the result of these millions of years of evolution.”

Source; http://actu.epfl.ch/

 

Simple Genetic Manipulation Could Extend Life 20%

By reducing the activity of one type of gene (mTOR), scientists said they increased the average life span of mice by about 20%, and preserved memory, cognition and other traits into old age. Though mouse studies don’t always translate to humans, Dr. Finkel, head of the laboratory of molecular biology in NIH‘s National Heart, Lung and Blood Institute and senior author of the new study said the results raise the possibility that targeting the gene with drugs that inhibit its activity might one day be at least part of a strategy for prolonging longevity in people. But researchers don’t know if whether inhibiting the action of the gene would have similar life-extending effects in humans, and if it did whether the benefit would come without unwanted problems.

singularity Drugs to slow aging through alterations to metabolism are not the path to radical life extension. Slowing aging does nothing for people already old. The research community should focus instead on rejuvenation through therapies that repair and remove the cellular damage that causes aging. The mice were bred to put out just 25 percent of the normal levels of mTOR protein, indicating that suppressing the activity of the gene “clearly makes mice live longer,” said Toren Finkel.
Source: http://www.cell.com/
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http://www.nhlbi.nih.gov/