Remote-control AMPK gene can delay aging

University of California at Los Angeles (UCLA) biologists found that when a gene is a major organ systems activated remotely, can slow down the aging process throughout the body.

Remote-control AMPK gene can delay aging

University of California at Los Angeles (UCLA) biologists found that when a gene is a major organ systems activated remotely, can slow down the aging process throughout the body.

In one experiment Drosophila, called life scientists started AMPK gene, a key gene in the cells of the energy sensor, decrease the energy level when the cell, the gene is activated.

The researchers found that increasing the amount of the gut when the Drosophila AMPK, which will increase the life of approximately 30% – from about six weeks to eight weeks – and Drosophila maintain healthy longer. The study published in the “Cell Reports” magazine September 4, 2014, and may have important implications for slow human aging and disease, David Walker said. He is an associate professor of integrative biology physiology at UCLA and is the senior author of the study.

“We have shown that when we activate AMPK intestinal or nervous system genes, we see slow down the aging process,” Walker said. This finding is important, because the extension of human life will probably need to protect the health of many organ systems of the body from the ravages of aging, but to the brain or other vital organs of the anti-aging treatment has been proven to have technical difficulties. Studies have shown that, in a more convenient organs activate AMPK, such as the intestine, may ultimately slow the aging process throughout the body, including the brain.

Walker said that humans have AMPK, but usually will not be activated at a high level in. “Instead, the study of aging-related diseases – Parkinson’s disease, Alzheimer’s disease, cancer, stroke, cardiovascular disease, diabetes – one by one, we think, AMPK may interfere with the aging process and delay many of these the onset of the disease, “said Walker, who is also a member of the Institute of Molecular Biology, University of California, Los Angeles. “We are still not enough evidence, of course, take years to prove that we as a goal, and we believe this is real. Ultimate goal of our research is to promote human healthy aging.”

Drosophila melanogaster is a good model for the study of human aging, because scientists have identified all the genes in the fruit fly, and know how to turn on and off individual genes. Biologists in the research process about 100,000 studied Drosophila.

The first author, a doctoral student Walker lab Matthew Ulgherait, focusing on a cellular process called autophagy, the process enables the cell degradation, and discard the old, damaged cellular components. Before cells are damaged by get rid of “cell trash”, autophagy prevents aging, and AMPK is activated proven in previous studies of this process.

Ulgherait study whether AMPK activation in Drosophila autophagy occurs can lead to speed faster than usual. “It’s an interesting finding that when AMPK Ulgherait activation of the nervous system, he found evidence that elevated levels of autophagy occurs not only in the brain, and intestine also happen,” Walker said. “And vice versa: activation of AMPK in the gut, but also to raise the level of autophagy brain – may also occur in other places.”

Walker pointed out that many neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s, are associated with the accumulation of protein aggregates related protein aggregates in the brain of a cell is garbage. “Ulgherait beyond its relevance and to establish a causal relationship,” he said. “Ulgherait pointed out that activation of autophagy against aging has a certain role, and he can bypass AMPK directly targeting autophagy.”

Walker said, AMPK is considered to be the main target of metformin, which is a drug used to treat type 2 diabetes, and metformin activates AMPK.

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