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NOTE FROM TED: Please do not look to this talk for medical advice. This talk only represents the speaker’s personal views and understanding of aging which remains an emerging field of study. We’ve flagged this talk because it falls outside the content guidelines TED gives TEDx organizers. TEDx events are independently organized by volunteers. The guidelines we give TEDx organizers are described in more detail here: http://storage.ted.com/tedx/manuals/tedx_content_guidelines.pdf

Could we reverse epigenetic aging by re-growing the thymus? In the future, will it be possible to extend our lives or increase our longevity? Dr. Greg Fahy is a low-temperature biologist and investigator of aging intervention in humans. His first clinical trial, intended to reverse immune system aging, provided evidence that aging could be reversed in humans. Dr. Greg Fahy is a low-temperature biologist and investigator of aging intervention in humans. His first clinical trial, intended to reverse immune system aging, provided the first evidence that global aging can be reversed in humans. This talk was given at a TEDx event using the TED conference format but independently organized by a local community.

A desirable option would be to use CRISPR gene editing to essentially cut out the unwanted gene. There are, however, many challenges ahead.


If you want to remove an undesirable gene from a population, you have a couple theoretical options — one that most people might find unthinkable, and one that lies outside our current scientific abilities.

The first involves locating a group of people without a particular gene and designing breeding programs around them. It would mean mating people in ways that society would consider incestuous. And we’ve seen the difficulties that result from that in the past — marriages between close relatives were a notorious cause of hemophilia in European royal families, for example.

A much more desirable option would be to use CRISPR gene editing to essentially cut out the unwanted gene. There are, however, many challenges ahead for such a strategy. Chief among them is the need to find mutations that, by themselves, are linked to particular diseases or disorders. And then we need guarantees that CRISPR will edit the correct genes.

Researchers have used the gene-editing technique CRISPR to delete a segment of DNA associated with autism and schizophrenia from mouse brain cells.

The technique has only proven effective in mice so far but may eventually be suitable for treating brain conditions in people, says Xiao-hong Lu, assistant professor of pharmacology and neuroscience at Louisiana State University Health in Shreveport.

Unlike techniques used to manipulate DNA in the mouse brain, CRISPR can be applied to people. He says, “We need a tool to help us to carry the genetic elements into the [human] brain.”

“We were very pleased to find out that even though life span is a very complicated trait caused by variation on a large number of loci, which is true for most complex traits, the number of loci that are in common is a totally finite number. So, we can imagine going on to the next stage and investigating one gene at a time and in combination,” Mackay said.


Scientists believe about 25 percent of the differences in human life span is determined by genetics—with the rest determined by environmental and lifestyle factors. But they don’t yet know all the genes that contribute to a long life.

A study published March 5, 2020, in PLOS Biology quantified variation in life span in the fruit fly genome, providing valuable insights for preserving health in elderly humans—an ever-increasing segment of the population. The paper titled “Context-dependent genetic architecture of Drosophila life span” is the culmination of a decade of research by Clemson University geneticists Trudy Mackay and Robert Anholt.

It remains difficult to address the for life span in humans, so researchers conduct their experiments with model systems. Mackay, the Self Family Endowed Chair of Human Genetics, is one of the world’s leading experts on the Drosophila melanogaster model (aka the common fruit fly), which is an excellent model for comparative analysis of human disease and aging. About 70 percent of the fruit fly genome has a human counterpart.

Circa 2017


Insulin-producing cells have been restored in mouse models of type 1 diabetes using a new genetic engineering technique.

American scientists adapted the gene editing technology known as CRISPR (clustered, regularly interspaced, short palindromic repeat) to successfully treat mouse models of type 1 diabetes, kidney disease and muscular dystrophy.

CRISPR enables scientists to edit the genetic material of an organism allowing for DNA sequences to be easily altered and gene function to be modified.

Circa 2013

These patents form part of Regeneron’s global patent portfolio, which together protect fundamental inventions behind Regeneron’s VelocImmune humanized mice. The two patents listed above specifically contain claims covering genetically modified mice that have unrearranged human immunoglobulin variable region gene segments at endogenous mouse immunoglobulin loci. The VelocImmune mice contain the full repertoire of human heavy chain immunoglobulin genes and kappa light chain genes, each linked to endogenous mouse constant regions. As a result, VelocImmune mice generate a normal and robust immune response which many believe is becoming the gold standard for making human antibody therapeutics. VelocImmune is also proving to be one of the most valuable technologies in biotechnology history, in terms of the licensing and collaboration revenues it has helped generate.


TARRYTOWN, N.Y., Aug. 7, 2013 /PRNewswire/ — Regeneron Pharmaceuticals, Inc. (NASDAQ: REGN) today announced that the United States Patent and Trademark Office granted U.S. Patent No. 8,502,018 relating to methods of genetically modifying a mouse to make human antibodies. A similar European.

Working around the clock for two weeks, a large team of Stanford Medicine scientists has developed a test to detect antibodies against the novel coronavirus, SARS-CoV-2, in blood samples.

In contrast to current diagnostic tests for COVID-19, which detect genetic material from the virus in respiratory secretions, this test looks for antibodies to the virus in plasma, the liquid in blood, to provide information about a person’s immune response to an infection.

The test was launched April 6 at Stanford Health Care. It differs from an externally developed test that Stanford researchers used for a prevalence study during recent community screening events.