Researchers Working to Improve Longevity

- February 8th, 2016

Recently two longevity studies have shown some promise in the age-old battle of old age.

It is well known that with age the risk of age-related illnesses like Alzheimer’s and cardiovascular disease increases. But what if scientists were able to curb the aging process?
Recently two studies have shown promise in the age-old battle of old age. While one study looks at the genetic structure of aging, the other looks at erasing age at a cellular level.

Genetics and longevity

University of Georgia scientists believe that they have identified that a hormone, instrumental in the aging process, is under genetic control. That discovery, outlined in a study, has opened up the train of thought that genetics dictates aging and diseases.
In 2014, it was discovered that upon restoration, the hormone GDF11 can reverse cardiovascular aging in old mice and can also lead to muscle and brain rejuvenation. Now, the University of Georgia scientists have found that levels of GDF11 are determined by genetics; that represents “another potential mechanism by which aging is encoded in the genome.”

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Rob Pazdro, an assistant professor in the college’s department of foods and nutrition, as well as the study’s senior author, commented, “[f]inding that GDF11 levels are under genetic control is of significant interest. Since it is under genetic control, we can find the genes responsible for GDF11 levels and its changes with age.”
Continuing, he equated the discovery to finding a “missing piece of the aging/genetics puzzle.” He believes the latest development is “an important step toward learning about aging and why we age and what are the pathways that drive it.”

Removing cellular clutter

While the scientists discussed above are looking to genetics as the answer to the aging process, researchers at the Mayo Clinic College of Medicine in Minnesota have found that when aged cells are removed from mice, the rodents live longer and benefit from healthier organ functions.
Darren Baker, a coauthor of the study, has explained that the procedure entailed removing aged senescent cells from middle-aged mice. “[A]fter six months of treatment, the treated animals were more exploratory, more active. They had also improvements in kidney function, in heart function,” he said.
Senescent cells are “cells that the researchers investigated in the study are dysfunctional cells that have stopped dividing, and whose presence has been linked to age-dependent diseases.” These cells accumulate with age in natural tissues.

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What is promising is that the findings “demonstrate that the removal of senescent cells does indeed delay aging and increase healthy life span,” said Jan van Deursen, chair of biochemistry and molecular biology at the Mayo Clinic.
Given the results, “this approach may be useful to treat aspects of age-related functional decline, age-related diseases that involve senescent cells or side effects of therapies that create senescent cells,” the researchers have noted.

Indeed, according to Baker, “[i]f translatable, because senescent cells do not proliferate rapidly, a drug could efficiently and quickly eliminate enough of them to have profound impacts on healthspan and lifespan.”
 
Securities Disclosure: I, Vivien Diniz, hold no direct investment interest in any company mentioned in this article.

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